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									                                  EUR CONFERENCES

                    Infections and lung diseases
                                        Paris, June 8-9, 2006

           Infections et maladies pulmonaires
                                         Paris, 8-9 juin 2006
                          Jean-Michel ALONSO, Institut Pasteur, Paris, France
                           Alice PRINCE, Columbia University, New York, USA
       Jean-Michel SALLENAVE, MRC Centre for Inflammation Research, Edinburgh, United Kingdom
                           Lhousseine TOUQUI, Institut Pasteur, Paris, France

                                  SCIENTIFIC DIRECTOR OF THE EURΩCONFERENCES

                                Jean-Marc CAVAILLON, Institut Pasteur, Paris, France

Institut Pasteur – Centre d’Information Scientifique – 28, rue du Docteur Roux – 75724 Paris Cedex 15, France
                           E-mail: euroconf-ip@pasteur.fr - Fax : 33 (0)1 40 61 30 25
   PATHOGENS                                                                                          AND THE CF LUNG
Human mucosal surfaces are often colonized with a wide array of microorganisms simul-              Dysregulated neutrophilic inflammation and chronic infection
taneously.The epithelial cells that line these spaces act as a physical barrier and also play a    lead to progressive destruction of the airways in cystic fibro-
vital role in the initiation of local innate immune responses. Polymicrobial stimulation of air-   sis. The lipoxins are endogenous anti-inflammatory lipid
way epithelial cells in vitro or in vivo with two mucosal pathogens, S. pneumoniae and H.          mediators that are important for immune counter-regula-
influenzae, leads to synergistic induction of proinflammatory signaling, and the resultant         tion in the lung. Recent data indicate that there is a patho-
local recruitment of neutrophils influences the outcome of interbacterial competition.             physiologically important defect in lipoxin-mediated anti-
Epithelial sensing of combinations of bacteria, as are commonly encountered during colo-           inflammatory activity in the cystic fibrosis airway, suggesting
nization, can drastically alter local inflammatory responses and determine the outcome of          novel approaches to pathogenesis and therapy in this lethal
competition between bacterial species. Interventions such as vaccination or antibiotic ther-       genetic disease.
apy that target specific members of the respiratory flora may inadvertently alter the              Christopher Karp, University of Cincinnati, USA
dynamics of complex microbial communities.
Adam J. Ratner, University of Pennsylvania, Philadelphia, USA
                                                                                                   3 COMPLEMENT ANAPHYLATOXINS
                                                                                                      AND RECEPTORS IN LUNG HOST DEFENSE
3 IMMUNE DEFENSES IN THE RESPIRATORY EPITHELIUM                                                    The C3a and C5a molecules play complex roles in host
The airway mucosa is mainly covered by a thin specialized epithelium, constituting a               defense. In some instances, C5a is requisite for acute clearance
vulnerable barrier, continuously being bombarded by exogenous antigens including poten-            of bacteria. However, overactivation of C5a receptors is asso-
tially infectious agents. Adequate mucosal protection depends on intimate                          ciated with progression of the systemic inflammatory response
co-operation between adaptive immunity and innate defense mechanisms such as mucus                 syndrome. While usually associated with bone marrow derived
and the ciliary function. Adaptive surface defense is primarily mediated by secretory IgA          cells, massive upregulation of C3a and C5a receptors occurs on lung epithe-
but also by potentially proinflammatory serum-derived and locally produced IgG                     lium following exposure to LPS.The therapeutic potential of antagonizing the anaphlyatoxin
antibodies. Mucosally induced regulatory mechanisms aim at avoidance of excessive inflam-          receptors in chronic lung diseases associated with infection, such as COPD and Cystic
mation and the commensal microbiota contributes to homeostatic control. There is cur-              Fibrosis, will be discussed.
rently considerable interest in exploiting the mucosal route both for anti-infective vaccines      Craig Gerard, Harvard Medical School, Boston, USA
and immunotherapy and there is a need for more basic knowledge to this end.
                                                                                                   3 THE ROLE OF THE NADPH OXIDASE IN THE KILLING OF BACTERIA
Per Brandtzaeg, University of Oslo, Norway                                                            AND FUNGI BY NEUTROPHILS - REPLACING THE PARADIGM OF FREE
   TO S.AUREUS AND P.AERUGINOSA                                                                    The NADPH oxidase plays an essential role in the killing of bacteria and fungi by neu-
Airway epithelial cells are an important component of the mucosal immune system initiat-           trophils. Defects in this oxidase or an anaerobic environment impairs killing. The oxidase
ing the innate immune response to inhaled pathogens. To cope with the diverse types of             produces copious amounts of superoxide, which, together with other "reactive oxygen
bacterial pathogens specific receptor complexes are actively mobilized to the apical sur-          species" was thought to directly kill the microbes.This is not the case.The oxidase gener-
faces of airway cells and presented in conjunction with signaling kinases, within the context      ates a charge across the wall of the phagocytic vacuole that pumps ions across the mem-
of lipid rafts. AsialoGM1 and TLR2 are co-receptors capable of recognizing and initiating          brane. Cl- is pumped out of, and K+ into, the vacuole which, together with activation of type
NF- B dependent gene transcription in response to both Gram-negative and Gram-posi-                1 Na+/H+ exchanger which exchanges Na+ in the vacuole for H+ in the cytoplasm, activate
tive organisms.TNFR1 is mobilized in response to staphylococcal protein A initiating TNF           the microbicidal enzymes released into the vacuole from the cytoplasmic granules.
signaling in response to a discrete ligand. Multiple signaling cascades may be initiated by bac-   Anthony W. Segal, University College London, United Kingdom
terial ligands in sufficient quantity to activate these receptors.                                 3 DEFENSINS AND THE LUNG: PAST, PRESENT AND FUTURE
Alice Prince, Columbia University, New York, USA                                                   Defensins are small, cysteine-rich peptides with a long past and an intriguing future.
3 PULMONARY INFECTIONS AND TOLL-LIKE RECEPTORS                                                     Produced by plants, fungi, invertebrates and vertebrates, defensins are endogenous, gene-
                                                                                                   encoded antibiotics that contribute substantially to innate mucosal immunity. At least eight
The Toll-like receptors (TLR) are important for the innate immune response of the host to          different defensin peptides help protect the human lungs: four beta-defensins (HBD 1-4)
infections.Their main function is to sense pathogens and to trigger a cascade of events lead-      and four alpha defensins (HNP 1-4). We will describe their structures, summarize their
ing to the expression of inflammatory molecules useful for an early acute defense but harm-        antimicrobial and antiviral properties, and suggest how they work. We will introduce the
ful when produced in excess. As lungs are constantly exposed to airborne pathogens, the            fascinating theta defensins (cyclic minidefensins) of nonhuman primates, and end by dis-
innate host defense is of particular importance.TLR are expressed at the lung level by dif-        cussing the prospects of using defensins as therapeutic agents in the future.
ferent cell types, including alveolar macrophages and respiratory epithelial cells.Their role      Robert I. Lehrer, UCLA, Center for the Health Sciences, Los Angeles, USA
for the fight of bacteria, fungi and viruses is evident but not univocal.
Michel Chignard, Institut Pasteur, Paris, France                                                   3 ANTIMICROBIAL PEPTIDES IN THE RESPIRATORY TRACT:
                                                                                                      ROLE IN INFECTION, INFLAMMATION AND IMMUNITY
3 TOLL-LIKE RECEPTOR SENSING AND CONTROL OF INTRACELLULAR                                          The innate immune system is an essential line of defence against respiratory infections.
   PATHOGENS                                                                                       Antimicrobial peptides that are produced by the epithelial cells lining the airways and the
Microbes and their products are sensed by cells of the innate immune system through Toll-          neutrophils are important contributors to this line of defence because they display antimi-
Like receptors (TLR). Pathogen induced activation of antigen presenting cells recruits lym-        crobial activity against a range of micro-organisms. It is now recognized that these mole-
phocytes to mount an adaptive immune response with effective elimination of the                    cules not only kill inhaled bacteria, fungi and viruses, but also display other functions in
pathogen.The role TLR mediated sensing and activation has been investigated for G+ and             immunity and wound repair by activating a range of cell types, including neutrophils, den-
G- bacteria, fungi, parasites and viruses. Our team focussed on Mycobacterium tuberculosis         dritic cells and epithelial cells.This talk will address these new insight into the central role
(MTB) infection using mice deficient for the common TLR adaptor protein, MyD88,                    of antimicrobial peptides in the lung.
involved in TLR signalling. MyD88 -/- macrophage do not respond to mycobacteria, display           Pieter S. Hiemstra, Leiden University Medical Center,The Netherlands
reduced phagocytosis and defective killing of bacilli. Aerosol infection of MyD88 -/- mice
with MTB (100CFU) is lethal within 4 weeks with 3 log higher CFU in the lung and acute,            3 GENETIC PROGRAMS REGULATING HOST DEFENSE OF THE LUNG
necrotic pneumonia despite the induction of an adaptive immunity. Similar data are                 A complex transcriptional program coordinately regulates the expression of molecules
obtained for another intracellular pathogen, Listeria monocytogenes.These data suggest that        mediating innate immunity and pulmonary surfactant that are required for lung homeosta-
TLR/MyD88 signalling plays a critical role for the activation of the innate immune system          sis. Activation of these transcriptional programs are, in turn, influenced by signaling mole-
by MTB or Listeria, while the generation of an adaptive immune response is TLR inde-               cules including growth factor and cytokines that enhance cell survival and induce the syn-
pendent.                                                                                           thesis of innate host defense molecules including the surfactant collectins, SP-A and SP-D.
Bernhard Ryffel, Institut Transgenose, Orléans, France                                             Jeffrey A.Whitsett, Cincinnati Children’s Hospital Medical Center, Cincinnati, USA

   IMMUNITY                                                                                           AND HOST DEFENSE
Successful host defenses against invading pathogens require coordinated interactions               In the course of evolution, the surfactant protein (SP-) A, an innate host defense molecule,
between innate and adaptive immunity. IL-12 and IL-23 are myeloid derived heterodimeric            acquired progressively genetic and epigenetic complexity. This may, in specific, reflect the
cytokines which regulate specific aspects of innate and adaptive immunity in the lung. IL-12       importance of SP-A as innate host defense molecule and, in general, the need for a more
is required for regulation of Th1 responses and host defense against intracellular                 diverse host defense system, as one moves up the evolutionary ladder. In the presentation,
pathogens, whereas IL-23 is required for ThIL-17 responses and host defense against extra-         I will discuss the different types of SP-A complexity, and regulatory and functional differ-
cellular Gram negative bacteria in the lung. The regulation of IL-12 and IL-23 as well as          ences among SP-A variants with focus on the differential ability of human SP-A variants to
downstream mediators of host defense, in the context of pulmonary infection, will be pre-          enhance phagocytosis of P. aeruginosa by macrophages. Mechanisms and working models
sented.                                                                                            may also be discussed.
Jay K. Kolls, Children's Hospital of Pittsburgh, USA                                               Joanna Floros, The Pennsylvania State University, Hershey, USA
                                                                                                                                           PA R I S , J U N E 8 - 9 2 0 0 6

                    3 CONTAGION: PERSON-TO-PERSON SPREAD                                          appears to play a critical role in determining the severity of acute lung injury, in part
                       OF RESPIRATORY INFECTIONS                                                  because lung epithelial injury slows the resolution of alveolar edema. Novel treatments are
                         Contagion of respiratory organisms depends upon biological fac-          being developed that may attenuate the severity of bacterial-induced lung injury and pro-
                          tors that affect the capacity of an organism to proliferate in the      mote the resolution of acute respiratory failure.
                           airways and spread via secretions, and the size of the inoculum        Michael A. Matthay, University of California, San Francisco, USA
                            that leads to colonization and/or infection of another person.        3 CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)
                            There are surprising differences among organisms.Three general           INFECTION/EXACERBATIONS
                             patterns will be discussed, and specific clinical and/or experi-
                             mental examples will be provided, citing a range of organisms.       COPD is a condition characterised by several distinct phenotypes and intermittent
                            Streptococcus pneumoniae, for example, spreads from one person        episodes of worsening (exacerbations). Furthermore, it is recognised as an “inflammatory
                            to another generally by direct contact with nasopharyngeal            disease” which is central to its progression.The role of infection has been unclear because
                           secretions, but does not directly produce infection; rather, a stage   some patients have bacteria in the lower airways continuously (colonisation) and the inci-
                          of colonization and proliferation in the upper airways may be fol-      dence doesn’t change much during exacerbations. However recent data confirms the size
                         lowed by development of infection (e.g., otitis media, sinusitis or      of the colonising load influences inflammation (1) and the load increases (2) and bacterial
                        pneumonia), with many host factors influencing the likelihood of          phenotype changes (3) during exacerbations with increased inflammation (episodes with
                      such an occurrence. In contrast, influenza virus aerosolizes; inhalation    purulent sputum).These findings may explain some of the progression of COPD.
                   after a single exposure may be followed immediately by infection in a          Robert Stockley, Queen Elizabeth Hospital, Birmingham, United Kingdom
                substantial proportion of exposed persons if they are not specifically            3 TUBERCULOSIS:A SUBTLE EQUILIBRIUM BETWEEN A PATHOGEN
              immune to the infecting type. Finally, Mycobacterium tuberculosis also                 AND ITS HOST
        aerosolizes and the infection rate may be quite high but, unlike the situation with
 influenza, exposure tends to be prolonged. However, most infection is subclinical, so that       Tuberculosis is a complex disease caused by M. tuberculosis. One bacteria infects one
contagion may be undetected; disease then occurs each year in a certain proportion of             macrophage present in one alveolus anywhere in the lung. In absence of immune response
those persons who have had subclinical infection. Patterns of contagion by other bacterial        the bacteria will growth unlimited, kill the infected subject, but disappear at his death. At
and viral organisms will be compared and contrasted to these three examples.                      the opposite the immune response recruits numerous T-cells that create inflammatory foci
Daniel M. Musher, Baylor College of Medicine, Houston, USA                                        able to restrict bacterial growth.The infection stops at this stage, 90/95% of subjects are
                                                                                                  sensitised but not ill.The bacteria will also disappear. Pulmonary tuberculosis occurs only
3 NOSOCOMIAL PNEUMONIA: KILLER, OR MARKER OF SEVERITY                                             in some subjects. A cavity appears in a given lung inflammatory focus. Rare bacteria that
Nosocomial pneumonia (NP) is a frequent event in severe patients, in particular after aspi-       have persisted in quiescent form during months or years are able to growth in the necrotic
ration, surgical procedures, and mechanical ventilation with intubation or tracheotomy. In        tissues.The bacteria are save, able to contaminate new subjects around the diseased per-
this last group of patients, when intubation stays more than 3 days, incidence is up to 20        son. The immune response creates conditions for the species survival. M. tuberculosis is
to 30%. People use the term VAP (ventilator associated Pneumonia), but it is unfortunate,         totally dependant of human beings and of their immune responses.
since NP is due to the disease which made the intubation necessary, rather than to the            Gilles Marchal, Institut Pasteur, Paris, France
tube itself. NP is consirered as a very serious event, responsible for a high mortality, and      3 MODELS OF LUNG INFECTIONS IN MICE: USE OF ADENOVIRUS VECTORS
possibly related to a poor quality of care. It is clear in the literature that crude mortality
of this event is very high (40 to 50%), but controversies persist on the real attributable           CODING FOR ANTIMICROBIAL MOLECULES FOR THERAPEUTIC
mortality of this infectious event, and on the possibility to prevent it. In some settings, the      AND VACCINATION STRATEGIES
event is related to an aspiration which happened before admission in the hospital, or the         Endogenous antimicrobial molecules (EAMs) are evolutionarily ancient elements of the
ICU (severe trauma, coma of any origin, end of life...). In those cases, it is easy to under-     host defense system against infections that can be found in animals, plants and bacteria.
stand that NP is a marker of severity, rather than a quality indicator. One issue is that we      In addition to killing micro-organisms, antimicrobial molecules contribute to innate
don't know how long it could take to develop NP after aspiration. It could be due to the          immune host defense activities (chemotactic, immunostimulatory and mitogenic). In par-
inoculum and the host defenses. For late NP, some preventive measures showed some effi-           ticular, EAMs can use a variety of receptors on innate and immune eukaryotic cells to acti-
cacy (Prophylactic antibiotics, semi recumbent position in the bed...). However, many NP          vate adaptive immunity. Recently, adenovirus vectors have been used to over-express EAMs
occur although preventive measures have been taken, and do not seem to be related to              (such as cathelicidin and elafin) in the protection of mice against lung infections
quality of care. Host defenses, in particular in the lung, and the immunodepression which         (Staphylococcus aureus, Pseudomonas aeruginosa).We also propose that these molecules may
happens frequently after severe infections are probably risk factors, but this remains to be      be useful as potential adjuvants in vaccination strategies.
demonstrated.                                                                                     Jean-Michel Sallenave, MRC Centre for Inflammation Research, Edinburgh, United Kingdom
Jean Carlet, Fondation Hôpital St Joseph, Paris, France
                                                                                                  3 INTERVENTION STRATEGIES FOR NEWLY EMERGING RESPIRATORY
3 DO CHILDHOOD RESPIRATORY INFECTIONS PREVENT, CAUSE,                                                VIRUSES
   OR MERELY REVEAL ASTHMA?                                                                       In the past decades, we have been confronted with an increasing number of newly emerg-
Viral respiratory infections have long been associated with wheezing illnesses and asthma         ing virus infections, many of these are caused by respiratory viruses like SARS-CoV, avian
in childhood, but the nature of this relationship is debated.While on one hand, severe RSV        influenza viruses and hMPV.With the advent of modern technology, our possibilities for the
illnesses appear to increase the risk of asthma, evidence related to the hygiene hypothesis       development of early warning systems and preparedness plans have increased significantly,
suggests that infections can prevent asthma. Finally, one of the most difficult questions to      allowing us to rapidly develop adequate intervention strategies. These include the use of
address is whether infections really change the risk of asthma, or alternatively, are simply      surveillance, antiviral strategies and vaccination.An overview will be given of the strategies
indicators. Although definitive resolution of these questions await the development of            that are currently needed to combat these newly emerging infections efficiently.
practical anti-viral interventions, new data will be presented to help reexamine these            Albert D.M.E. Osterhaus, Erasmus MC, Rotterdam,The Netherlands
fundamental questions about viruses, wheezing, and asthma.
James E. Gern, University of Wisconsin, Madison, USA
                                                                                                  3 VIRAL-VECTORED RESPIRATORY MUCOSAL IMMUNIZATION STRATEGIES
                                                                                                     AGAINST TUBERCULOSIS
3 PATHOGENESIS OF INFLAMMATION AND INFECTION IN CYSTIC                                            Pulmonary tuberculosis (TB) remains one of the leading infectious causes of death.While
   FIBROSIS                                                                                       BCG vaccine is effective in controlling childhood TB, it is ineffective for adult TB.There is
The hallmarks of the lung pathology in Cystic Fibrosis (CF), are bacterial colonization of        an urgent need to develop heterologous vaccines that are able to effectively boost and sus-
the lung with Staphylococcus aureus and Pseudomonas aeruginosa, associated with an exag-          tain the protective immunity triggered by parenteral BCG prime immunization. We have
gerated, sustained and extended inflammatory response characterized by influx of neu-             developed recombinant adenovirus- and vesicular stomatitis virus-vectored TB vaccines
trophils and increased release of pro-inflammatory cytokines.This presentation will review        and our findings suggest that these viral platforms are very promising boost vaccines for
the factors that link the basic (CFTR mutation) defect of CF to the propensity of bacter-         BCG prime immunization in experimental models.
ial colonisation including the dehydration of the airway surface liquid and decreased mucus       Zhou Xing, McMaster University, Hamilton, Canada
transport, the increased luminal salt concentrations that inactive the antibacterial proteins,
the increased number of epithelial and mucin bacterial defense receptors and the failure of       3 SURFACE PROTEINS OF STREPTOCOCCUS PNEUMONIAE: THEIR ROLES
CFTR to ingest and clear bacteria. It has been also suggested that inflammation may pre-             IN VIRULENCE AND POTENTIAL AS VACCINES
cede infection, whether it is related to a constitutive NF- B abnormal expression or to a         Pneumococcal proteins may offer an alternative to the existing polysaccharide and poly-
defect in the generation of endogenous anti-inflammatory lipid mediators will be discussed.       saccharide-protein vaccines. If successful they should lower vaccine cost enough so that
Edith Puchelle, Inserm U514, CHU Maison Blanche, Reims, France                                    they can be used worldwide to help prevent the more than 1.4 million deaths in children
                                                                                                  and probably an equal number of deaths in the elderly. Many pneumococcal proteins have
3 ACUTE LUNG INJURY: MECHANISMS OF INJURY FROM BACTERIAL                                          been described that are necessary for full virulence. These proteins can reduce comple-
   INFECTION                                                                                      ment deposition, modify host molecules, damage host cells, and play roles in attachment
Bacterial infection is the most important cause of acute lung injury and acute respiratory        and invasion. Immunization with many of the proteins can cause significant protection in
failure in critically ill patients. Several mechanisms mediate bacterial-induced lung injury to   animal studies. Immunization with mixtures of them can result in complete protection.
both the lung endothelium and the alveolar epithelium. Injury to the alveolar epithelium          David E. Briles, University of Alabama, Birmingham, USA
                     Infections and lung diseases                                                     REGISTRATION - INSCRIPTION
                                                                                                                     Lung diseases
                                  Paris, June 8-9, 2006                                                        Infections pulmonaires
The 2006 EUR CONFERENCE on Infections and Lung Diseases will provide an update                       Please complete and return this form with
on the more advanced knowledge on the mechanisms of both innate and adaptative                                      your payment to:
immunity in the respiratory tract, as well as on the pathophysiology and therapeutic and
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both at the experimental and clinical levels.With more than 3 millions deaths each year,
pulmonary infectious diseases represent the first cause of mortality associated to infec-                     INSTITUT PASTEUR
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role(s) of differents cell types and mediators involved in the initation of inflammation
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and bacterial pneumonia, tuberculosis, infection-associated asthma, cystic fibrosis, or              Family Name / Nom :_____________________________
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                               - les pays de l’Union Européenne : compagnie et institution          et institution ayant un n° de TVA intracommunautaire et
                                 sans n° de TVA intracommunautaire                                - pour le RESTE DU MONDE
                                      Until May 9, 2006             After May 9, 2006                   Until May 9, 2006                  After May 9, 2006
                                     Avant le 9 mai 2006           Après le 9 mai 2006                 Avant le 9 mai 2006                Après le 9 mai 2006
         Academic                          450                              550                              376.25                            459.87                           Académique
         Industrial                      1 050                            1 250                              877.93                           1 045.15                          Industriel
         Student*                          150                              160                              125.42                            133.78                           Etudiant*
                                                       Voir la rubrique « Informations pratiques » de la conférence sur notre site Intranet                                    Pasteurien
         Group rate                                    20% Discount (3 people minimum) / Remise de 20% à partir de 3 personnes                                               Tarif de groupe
*Student: please provide a copy of your student card, signed by your research director.           *Etudiant : merci de joindre une copie de la carte d’étudiant de l’année, signée par le directeur de
 Students cannot benefit from the group discount.                                                 recherche. Les étudiants ne peuvent pas bénéficier du tarif groupe.

Our fees include documentation, coffee-breaks and luncheons.                                      Les frais d’inscription incluent la fourniture des documents, les pauses-café
You will be registered upon reception of the registration form along with your                    et les déjeuners. L’admission des participants se fera à réception du bulletin d’ins-
payment. Please note that payment is required in advance. A receipt will be sent                  cription dûment rempli, accompagné du règlement ou du bon de commande (pour
after the payment.                                                                                les organismes publics exclusivement). La facture acquittée correspondante vous
                                                                                                  sera ensuite adressée.
                                                                                                  3 ANNULATION
Cancellations must be sent by letter or via e-mail at least before May 9. In that
case registration fees will be reimbursed, except for an administrative charge of                 Toute notification de désistement doit nous parvenir par courrier ou e-mail avant le 9 mai.
90 euros.                                                                                         Dans ce cas, l’Institut Pasteur rembourse les frais d’inscription excepté 90 euros de frais de
If, despite its efforts, Institut Pasteur cancels an event, it is not responsible for any         dossier. Passée cette date, l’Institut Pasteur conservera l’intégralité des frais d’inscription.
airfare, hotel or other costs incurred by registrants. Speakers are subjected to                  En cas d’annulation de la manifestation par l’Institut Pasteur, celui-ci n’est pas respon-
change without notice.                                                                            sable des pertes dues aux annulations de transport, de réservations d’hôtel ou d’autres
                                                                                                  dépenses engagées par les participants. Les organisateurs se réservent le droit de modifier
3     DOCUMENTATION                                                                               le programme si malgré tous leurs efforts les circonstances les y obligent.
A summary of the conferences with copies of the most relevant illustrations and                   3 DOCUMENTATION
abstracts of the posters will be provided at the beginning of the conference,                     Les résumés des différentes interventions, incluant les illustrations les plus significatives
pending authors’ permission.                                                                      présentées par les conférenciers, et les résumés des présentations affichées, seront
3     ABSTRACTS SUBMISSION AND POSTERS                                                            fournis à chaque participant au début de la manifestation, sous réserve de l’autorisa-
                                                                                                  tion des auteurs.
Posters describing recent research results will be displayed during the conference,
after selection by the organisers of submited abstracts (250 words maximum).                      3 SOUMISSIONS DE RÉSUMÉS ET PRÉSENTATION D’AFFICHES
Please complete the abstract form directly on our website < http://pasteur.fr/                    Les affiches sélectionnées à partir des résumés (250 mots maximum) communiqués aux
applications/euroconf/lungdiseases> or eventually request camera ready profor-                    organisateurs et décrivant des résultats récents seront exposées pendant la conférence.
mata.The reception deadline is April 14, 2006.The decision (acceptance for oral                   Merci de compléter le formulaire directement sur notre site web (http://pasteur.fr/
presentation or poster) will be communicated before May 9, 2006. The final                        applications/euroconf/lungdiseases) ou éventuellement de nous le demander. La date
dimensions of posters are of 0.7 m width x 1 m high.The abstracts will appear in                  limite de réception des résumés est le 14 avril 2006. La décision (sélection pour pré-
the book distributed to the participants. Six abstracts will be selected for oral                 sentation orale ou affichage) sera transmise aux auteurs avant le 9 mai 2006. La
presentation.                                                                                     dimension finale des affiches sera de 0,70 m de large / 1 m de haut. Les résumés paraî-
3      STAND - BROCHURES INSERTION                                                                tront dans le livre remis aux participants. Six résumés seront sélectionnés pour une pré-
                                                                                                  sentation orale.
If you wish to exhibit at the meeting or advertise in the delegate’s documentation
pack by inserting brochures, do not hesitate to contact us.                                       3 STAND - INSERTION DE DOCUMENTS
E-mail : bobichon@pasteur.fr                                                                      Si vous désirez disposer d’un stand ou si vous voulez faire insérer des brochures dans
                                                                                                  les mallettes des participants, n’hésitez pas à nous contacter.
3    PROFESSIONAL TEACHING CONFERENCE                                                             E-mail : bobichon@pasteur.fr
These EURΩCONFERENCES are professional teaching conferences                                       3 FORMATION PROFESSIONNELLE CONTINUE
(N° 11752184675). At your request, you will receive an agreement form.
                                                                                                  Ces EUR CONFERENCES peuvent entrer dans le champ de la formation profession-
3     HOTEL                                                                                       nelle continue. Le numéro de déclaration d’existence est le N°11752184675. Sur
Hotels in the vicinity of the Institut Pasteur are ready to welcome you. Please                   demande, une convention vous sera adressée.
consult the list of hotels on our website:                                                        3 HÔTEL
<http://www.pasteur.fr/applications/euroconf/lungdiseases> and contact them directly              Des hôtels situés à proximité de l’Institut Pasteur peuvent vous recevoir. Une liste est
informing that you are a participant in our INSTITUT PASTEUR EUR CONFE-                           disponible sur notre site web :
RENCE. Early reservation is recommended.                                                          <http://www.pasteur.fr/applications/euroconf/lungdiseases>. Contactez directement
                                                                                                  l’hôtel de votre choix en signalant que vous participez à notre INSTITUT PASTEUR
                                                                                                  EUR CONFERENCE. Nous vous recommandons de réserver au plus tôt.

                                  Forms available on the website - Formulaires disponibles sur le site web
P                   R                     O                    G                      R                     A                    M                     M                       E
                                                           14:30 – 15:00                                                 10:30 – 11:00          COFFEE BREAK / PAUSE CAFÉ
      THURSDAY JUNE 8, 2006                                Complement anaphylatoxins and receptors in lung
        JEUDI 8 JUIN 2006                                  host defense                                                                  Exhibition and posters
                                                                                                                              Visite des stands et présentation des affiches
                                                           Les anaphylatoxines et récepteurs du complément dans
8:00 - 8:55                                                la défense innée pulmonaire                                                MAIN INFECTIONS (PART 2)
      REGISTRATION OF THE PARTICIPANTS                     Craig Gerard, Harvard Medical School, Boston, USA                       INFECTIONS MAJEURES (PARTIE 2)
          ACCUEIL DES PARTICIPANTS                         15:00 – 15:30                                                              Moderators / Modérateurs :
                                                                                                                                  Bruno Crestani & B. Boris Vargaftig
8:55 - 9:00                                                The role of the NADPH oxidase in the killing of
Presentation of the EURΩCONFERENCES                        bacteria and fungi by neutrophils - replacing the             11:00 – 11:30
                                                           paradigm of free radical damage with ion pumps and            Pathogenesis of inflammation and infection in cystic
Présentation des EURΩ CONFERENCES                          pH optimisation
Jean-Marc Cavaillon                                                                                                      fibrosis
                                                           Rôle de la NAPDH oxydase dans la destruction des bac-         La pathogénie de l’inflammation et de l’infection dans la
Scientific Director / Directeur Scientifique               téries et des champignons par les neutrophiles - Remise
Institut Pasteur EURΩ CONFERENCES, Paris, France                                                                         mucoviscidose
                                                           en place du paradigme des radicaux libres avec les            Edith Puchelle, Inserm U514, CHU Maison
             SESSION 1 : THE AIRWAYS                       pompes ioniques et l’optimisation du pH                       Blanche, Reims, France
               LES VOIES AÉRIENNES                         Anthony W. Segal, University College London,
            Moderators – Modérateurs :                     United Kingdom                                                11:30 – 12:00
         Jean-Michel Alonso & Alice Prince                 15:30 - 16:00                 TEA BREAK / PAUSE THÉ           Acute lung injury: mechanisms of injury from bacte-
                                                                                                                         rial infection
9:00 – 9:30                                                                Exhibition and posters                        L’atteinte pulmonaire aiguë : mécanismes des lésions
Epithelial inflammatory responses to respiratory                Visite des stands et présentation des affiches           induites par les infections bactériennes
bacterial pathogens                                                                                                      Michael A. Matthay, University of California, San
Réponses inflammatoires épithéliales aux bactéries               SESSION 3 : HOST DEFENSE DURING                         Francisco, USA
pathogènes pulmonaires                                                    LUNG INFECTION
Adam J. Ratner, University of Pennsylvania,                 DÉFENSE DE L’HÔTE AU COURS DE L’INFECTION                    12:00 – 12:30
Philadelphia, USA                                                           PULMONAIRE                                   COPD Infection/exacerbations
                                                                                                                         BPCO : infection/exacerbation
9:30 – 10:00                                                         Moderators – Modérateurs :
                                                                   Marie-Anne Gougerot-Pocidalo                          Robert Stockley, Queen Elizabeth Hospital,
Immune defenses in the respiratory epithelium                                                                            Birmingham, United Kingdom
Défense immunitaire de l’épithélium respiratoire                        & Lhousseine Touqui
Per Brandtzaeg, University of Oslo, Norway                 16:00 – 16:30                                                 12:30 – 13:00
10:00 – 10:30                                              Defensins and the lung: past, present and future              Tuberculosis: a subtle equilibrium between a patho-
                                                           Défensines et poumons : passé, présent et futur               gen and its host
Molecular mechanisms of epithelial signaling in res-                                                                     Tuberculose : un équilibre subtil entre le pathogène et
ponse to S. aureus and P. aeruginosa                       Robert I. Lehrer, UCLA, Center for the Health
                                                           Sciences, Los Angeles, USA                                    son hôte
Mécanismes moléculaires de la signalisation des cellules                                                                 Gilles Marchal, Institut Pasteur, Paris, France
épithéliales en réponse à S. aureus et P. aeruginosa       16:30 – 17:00
Alice Prince, Columbia University, New York, USA                                                                         13:00 – 14:15                    LUNCH / DÉJEUNER
                                                           Antimicrobial peptides in the respiratory tract: role
10:30 - 11:00          COFFEE BREAK / PAUSE CAFÉ           in infection, inflammation and immunity                                      Exhibition and posters
                                                           Les peptides anti-microbiens dans le tractus respira-             Visite des stands et présentation des affiches
                Exhibition and posters                     toire : rôle dans l’infection, l’inflammation et l’immunité
     Visite des stands et présentation des affiches        Pieter S. Hiemstra, Leiden University Medical
                                                           Center,The Netherlands                                        14:15 – 15:15
    SESSION 2 : IMMUNOLOGICAL FUNCTIONS                                                                                    Short communications selected from posters
      IN THE RESPIRATORY TRACT (PART 1)                    17:00 – 17:30
                                                           Genetic programs regulating host defense of the               Communications libres sélectionnées à partir des résumés
            RESPIRATOIRE (PARTIE 1)                        lung                                                                SESSION 5 : THERAPEUTIC STRATEGIES
                                                           Programme génétique régulant la défense pulmonaire                       STRATÉGIES THÉRAPEUTIQUES
           Moderators – Modérateurs :                      de l’hôte
    Annick Clément & Philippe-Henri Lagrange               Jeffrey A.Whitsett, Cincinnati Children’s Hospital                        Moderators – Modérateurs :
                                                           Medical Center, Cincinnati, USA                                      Jean-Michel Sallenave & Remy Teyssou
11:00 – 11:30
Pulmonary infections and Toll-like receptors               17:30 – 18:00                                                 15:15 – 15:45
Infections pulmonaires et récepteurs TLR                   Genetic polymorphism of human surfactant protein              Models of lung infections in mice: use of adenovirus
Michel Chignard, Institut Pasteur, Paris, France           A and host defense                                            vectors coding for antimicrobial molecules for the-
11:30 – 12:00                                              Polymorphisme génétique de la protéine A du surfactant        rapeutic and vaccination strategies
                                                           et la défense de l’hôte                                       Modèles d’infections pulmonaires chez la souris : utili-
Toll-Like Receptor sensing and control of intracel-        Joanna Floros, The Pennsylvania State University,             sation de vecteurs adénoviraux codant pour des molé-
lular pathogens                                                                                                          cules anti-microbiennes en vue d’une stratégie théra-
                                                           Hershey, USA
Détection et contrôle des pathogènes intra-cellulaires                                                                   peutique ou vaccinale
par les récepteurs TLR                                                                                                   Jean-Michel Sallenave, MRC Centre for
Bernhard Ryffel, Institut Transgenose, Orléans,                     FRIDAY JUNE 9, 2006                                  Inflammation Research, Edinburgh, United Kingdom
                                                                   VENDREDI 9 JUIN 2006                                  15:45 – 16:15
12:00 – 12:30                                                  SESSION 4 : MAIN INFECTIONS (PART 1)
Novel heterodimeric cytokines: master regulators                                                                         Intervention strategies for newly emerging respira-
                                                                 INFECTIONS MAJEURES (PARTIE 1)
                                                                                                                                                                                         Illustration : Marie Guibert - www.marieguibert.com

of lung immunity                                                                                                         tory viruses
Nouvelles cytokines hétérodimaires : principaux régula-              Moderators – Modérateurs :                          Stratégies d’intervention contre les virus respiratoires
teurs de l’immunité pulmonaire                                Dominique Israel-Biet & Sylvie van der Werf                émergents
Jay K. Kolls, Children's Hospital of Pittsburgh, USA                                                                     Albert D.M.E. Osterhaus, Erasmus MC,
                                                           9:00 – 9:30                                                   Rotterdam,The Netherlands
                                                           Contagion: person-to-person spread of respiratory
12:30 – 14:00                                              infections                                                    16:15 – 16:45            TEA BREAK / PAUSE THÉ
                                                           Contagion : propagation de personne à personne des
       GROUP PHOTO / PHOTO DE GROUPE                       infections pulmonaires                                                        Exhibition and posters
                                                           Daniel M. Musher, Baylor College of Medicine,                      Visite des stands et présentation des affiches
                  LUNCH / DÉJEUNER
                                                           Houston, USA                                                  16:45 – 17:15
                Exhibition and posters
     Visite des stands et présentation des affiches        9:30 – 10:00                                                  Viral-vectored respiratory mucosal immunization
                                                           Nosocomial pneumonia: killer, or marker of severity           strategies against tuberculosis
           IMMUNOLOGICAL FUNCTIONS                         Les pneumonies nosocomiales : facteurs de mortalité ou        Utilisation des vecteurs viraux comme stratégie d’immu-
      IN THE RESPIRATORY TRACT (PART 2)                    marqueurs de sévérité                                         nisation de la muqueuse respiratoire contre la tubercu-
          FONCTIONS IMMUNOLOGIQUES                         Jean Carlet, Fondation Hôpital St Joseph, Paris,              lose
      DU TRACTUS RESPIRATOIRE (PARTIE 2)                   France                                                        Zhou Xing, McMaster University, Hamilton, Canada
            Moderators / Modérateurs :
       Christophe Delclaux & Jacky Jacquot                 10:00 – 10:30                                                 17:15 – 17:45
                                                           Do childhood respiratory infections prevent, cause,           Surface proteins of Streptococcus pneumoniae: their
14:00 – 14:30                                              or merely reveal asthma?                                      roles in virulence and potential as vaccines
Lipid anti-inflammatory mediators and the CF lung          Les infections respiratoires chez l’enfant empêchent,         Les protéines de surface de Streptococcus pneumo-
Les médiateurs lipidiques anti-inflammatoires et pou-      induisent ou révèlent l’asthme ?                              niae : rôles dans la virulence et possibilités vaccinales
mons mucoviscidosiques                                     James E. Gern, University of Wisconsin, Madison,              David E. Briles, University of Alabama,
                                                                                                                                                                                     Janvier 2006

Christopher Karp, University of Cincinnati, USA            USA                                                           Birmingham, USA

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