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16 Innate Immunity Nonspecific Defenses of the Host Learning

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									16: Innate Immunity: Nonspecific Defenses
of the Host



Learning Objectives
1. Differentiate between innate and adaptive immunity.
2. Define toll-like receptors.
3. Describe the role of the skin and mucous membranes in innate immunity.
4. Differentiate physical from chemical factors, and list five examples of each.
5. Describe the role of normal microbiota in innate resistance.
6. Classify phagocytic cells, and describe the roles of granulocytes and monocytes.
7. Define differential white blood cell count.
8. Define phagocyte and phagocytosis.
9. Describe the process of phagocytosis, and include the stages of adherence and ingestion.
10. Identify six methods of avoiding destruction by phagocytes.
11. List the stages of inflammation.
12. Describe the roles of vasodilation, kinins, prostaglandins, and leukotrienes in inflammation.
13. Describe phagocyte migration.
14. Describe the cause and effects of fever.
15. List the components of the complement system.
16. Describe three pathways of activating complement.
17. Describe three consequences of complement activation.
18. Define interferons.
19. Compare and contrast the actions of a-IFN and b-IFN with g-IFN.
20. Describe the role of transferrins in innate immunity.
21. Describe the role of antimicrobial peptides in innate immunity.



New in this Edition
•   Toll-like receptors and dendritic cells are discussed.
•   New sections on transferrins and antimicrobial peptides are included.
•   A new Applications box describes serum and whole blood collection.


Chapter Summary
Introduction (p. 474)
1. The ability to ward off disease through body defenses is called immunity.
2. Lack of immunity is called susceptibility.


The Concept of Immunity (p. 475)
1. Innate immunity refers to all body defenses that protect the body against any kind of
   pathogen.
2. Adaptive immunity refers to defenses (antibodies) against specific microorganisms.
3. Toll-like receptors are proteins in plasma membranes of macrophages and dendritic cells.
   TLRs bind to invading microbes.


First Line of Defense: Skin and Mucous Membranes (pp. 476–
478)
1. The body’s first line of defense against infections is a physical barrier and nonspecific
   chemicals of the skin and mucous membranes.


Physical Factors (pp. 476–477)
1. The structure of intact skin and the waterproof protein keratin provide resistance to microbial
   invasion.
2. Some pathogens, if present in large numbers, can penetrate mucous membranes.
3. The lacrimal apparatus protects the eyes from irritating substances and microorganisms.
4. Saliva washes microorganisms from teeth and gums.
5. Mucus traps many microorganisms that enter the respiratory and gastrointestinal tracts; in
   the lower respiratory tract, the ciliary escalator moves mucus up and out.
6. The flow of urine moves microorganisms out of the urinary tract, and vaginal secretions
   move microorganisms out of the vagina.


Chemical Factors (pp. 477–478)
1. Sebum contains unsaturated fatty acids, which inhibit the growth of pathogenic bacteria.
   Some bacteria commonly found on the skin can metabolize sebum and cause the
   inflammatory response associated with acne.
2. Perspiration washes microorganisms off the skin.
3. Lysozyme is found in tears, saliva, nasal secretions, and perspiration.
4. The high acidity (pH 1.2–3.0) of gastric juice prevents microbial growth in the stomach.


Normal Microbiota and Innate Immunity (pp. 478–479)
1. Normal microbiota change the environment, which can prevent the growth of pathogens.


Second Line of Defense (pp. 479–496)
 1. If a microbe penetrates the first line of defense it encourages production of phagocytes,
    inflammation, fever, and antimicrobial substances.


Formed Elements in Blood (pp. 479–482)
 1. Blood consists of plasma (fluid) and formed elements (cells and cell fragments).
 2. Leukocytes (white blood cells) are divided into three categories: granulocytes (neutrophils,
    basophils, eosinophils, and dendritic cells), lymphocytes, and monocytes.
 3. During many infections, the number of leukocytes increases (leukocytosis); some infections
    are characterized by leukopenia (decrease in leukocytes). *Animation: Host Defenses. The
    Microbiology Place.


Phagocytes (pp. 483–486)
 1. Phagocytosis is the ingestion of microorganisms or particulate matter by a cell.
 2. Phagocytosis is performed by phagocytes, certain types of white blood cells or their
    derivatives.
Actions of Phagocytic Cells (pp. 483–484)
 3. Among the granulocytes, neutrophils are the most important phagocytes.
 4. Enlarged monocytes become wandering macrophages and fixed macrophages.
 5. Fixed macrophages are located in selected tissues and are part of the mononuclear phagocytic
    system.
 6. Granulocytes predominate during the early stages of infection, whereas monocytes
    predominate as the infection subsides.
The Mechanism of Phagocytosis (p. 484)
 7. Chemotaxis is the process by which phagocytes are attracted to microorganisms.
 8. The phagocyte then adheres to the microbial cells; adherence may be facilitated by
    opsonization—coating the microbe with serum proteins.
 9. Pseudopods of phagocytes engulf the microorganism and enclose it in a phagocytic vesicle to
    complete ingestion.
10. Many phagocytized microorganisms are killed by lysosomal enzymes and oxidizing agents.
Microbial Evasion of Phagocytosis (pp. 485–486)
11. Some microbes are not killed by phagocytes and can even reproduce in phagocytes.
12. Evasion mechanisms include M protein, capsules, leukocidins, membrane attack complexes,
    and prevention of phagolysosome formation. *Animation: Phagocytosis. The Microbiology
    Place.


Inflammation (pp. 486–490)
 1. Inflammation is a bodily response to cell damage; it is characterized by redness, pain, heat,
    swelling, and sometimes the loss of function.
 2. Acute inflammation is a short, intense response to infection; chronic inflammation is a
    prolonged response.
Vasodilation and Increased Permeability of Blood Vessels (p. 487)
 3. The release of histamine, kinins, and prostaglandins causes vasodilation and increased
    permeability of blood vessels.
 4. Blood clots can form around an abscess to prevent dissemination of the infection.
Phagocyte Migration and Phagocytosis (pp. 487–489)
 5. Phagocytes have the ability to stick to the lining of the blood vessels (margination).
 6. They also have the ability to squeeze through blood vessels (emigration).
 7. Pus is the accumulation of damaged tissue and dead microbes, granulocytes, and
    macrophages.
Tissue Repair (p. 489)
 8. A tissue is repaired when the stroma (supporting tissue) or parenchyma (functioning tissue)
    produces new cells.
 9. Stromal repair by fibroblasts produces scar tissue. *Animation: Inflammation. The
    Microbiology Place.


Fever (pp. 489–490)
 1. Fever is an abnormally high body temperature produced in response to a bacterial or viral
    infection.
 2. Bacterial endotoxins, interleukin-1, and alpha-tumor necrosis factor can induce fever.
 3. A chill indicates a rising body temperature; crisis (sweating) indicates that the body’s
    temperature is falling.


Antimicrobial Substances (pp. 490–497)
The Complement System (pp. 490–494)
 1. The complement system consists of a group of serum proteins that activate one another to
    destroy invading microorganisms. Serum is the liquid remaining after blood plasma is
    clotted.
 2. Complement proteins are activated in a cascade.
 3. C3 activation can result in cell lysis, inflammation, and opsonization.
 4. Complement is activated via the classical pathway, the alternative pathway, and the lectin
    pathway.
 5. Complement is deactivated by host-regulatory proteins.
 6. Complement deficiencies can result in an increased susceptibility to disease.
 7. Some bacteria evade destruction by complement by means of capsules, surface lipid–
    carbohydrate complexes, and enzymatic destruction of C5a. *Animation: The Complement
    System. The Microbiology Place.


Interferons (pp. 494–496)
 8. Interferons (IFNs) are antiviral proteins produced in response to viral infection.
 9. There are three types of human interferon: a-IFN, b-IFN, and g-IFN. Recombinant interferons
    have been produced.
10. The mode of action of a-IFN and b-IFN is to induce uninfected cells to produce antiviral
    proteins (AVPs) that prevent viral replication.
11. Interferons are host-cell–specific but not virus-specific.
12. Gamma-interferon activates neutrophils and macrophages to kill bacteria.
Transferrins (p. 496)
13. Transferrins bind iron.


Antimicrobial Peptides (pp. 496–497)
14. Antimicrobial peptides lyse microbial cells.



The Loop
If you prefer to include the complement system with antigen–antibody reactions, pages 490–494
can be assigned with Chapter 17. Review questions 12, 13, 14, and Critical Thinking question 3,
concerning complement, can be assigned when complement is covered.


Answers
Review
1. a.     The ability of the human body to ward off diseases.
     b.   The lack of resistance to an infectious disease.
     c.   Host defenses that tend to protect the body from any kind of pathogen.
2.                                   Mechanical                                Chemical
      Skin                           Dry, packed cells                         Sebum
      Eyes                           Tears                                     Lysozyme
      Digestive tract                Movement out                              HCl
      Respiratory tract              Ciliary escalator
      Urinary tract                  Movement out
      Genital tract                  Movement out                              Acidic in female
3. See Table 16.1.
4. Phagocytosis is the ingestion of a microorganism or any foreign particulate matter by a cell.
5. Granulocytes have granules in the cytoplasm. Among the granulocytes, neutrophils have the
   most prominent phagocytic activity. Monocytes are agranulocytes (without granules) that
   develop into macrophages.
     When an infection occurs, granulocytes migrate to the infected area. Monocytes follow the
     granulocytes to the infected tissue. During migration, monocytes enlarge and develop into
     actively phagocytic cells called macrophages. Macrophages phagocytize dead or dying
     bacteria.
6. Phagocytic cells that migrate to the infected area are called wandering macrophages. Fixed
   macrophages remain in certain tissues and organs.
7. Refer to Figures 16.7 and 16.8.
8. Inflammation is the body’s response to tissue damage. The characteristic symptoms of
   inflammation are redness, pain, heat, and swelling.
9. The functions of inflammation are:
     1.   To destroy the injurious agent, if possible, and to remove it and its by-products from the
          body;
     2.   If destruction is not possible, to confine or wall off the injurious agent and its by-products
          by forming an abscess;
     3.   To repair or replace tissues damaged by the injurious agent or its by-products.
10. Leukocytic pyrogen, released from phagocytic granulocytes, has the ability to raise body
    temperature. The higher temperature is believed to inhibit the growth of some
    microorganisms. The higher temperature speeds up body reactions and may help body
    tissues to repair themselves more quickly.
11. The chill is an indication that body temperature is rising. Shivering and cold skin are
    mechanisms for increasing internal temperature. Crisis indicates body temperature is falling.
    The skin becomes warm as circulation is returned to it when the body attempts to dissipate
    extra heat.
12. Complement is a group of proteins found in normal blood serum. The classical pathway is
    activated by an antigen-antibody complex and C1 (see Figure 16.12). The alternative pathway
    is activated by microbial lipid-carbohydrate complex and factor B, factor D, and factor P (see
    Figure 16.13). The lectin pathway is initiated by carbohydrate-binding proteins (lectins)
    binding the mannose on microbes (see Figure 16.14).
13. Activation of complement can result in immune adherence and phagocytosis, local
    inflammation, and cell lysis.

     14. Endotoxin binds C3b, which activates C5–C9 to cause cell lysis. This can result in free cell
     wall fragments, which bind more C3b, resulting in C5–C9 damage to host cell membranes.
15. Interferons are antiviral proteins produced by infected cells in response to viral infections.
    Alpha-IFN and b-IFN induce uninfected cells to produce antiviral proteins. Gamma-IFN is
    produced by lymphocytes and activates neutrophils to kill bacteria.


Critical Thinking
1.   Transferrin binds available iron so bacteria can’t have it to grow. A bacterium might respond
     with increased siderophores to take up iron.
2.   The inflammatory response is usually a beneficial response. Exceptions to this are
     hypersensitivities and autoimmune diseases, which are discussed in Chapter 19. Each of the
     drugs has side effects; while reducing inflammation, another undesirable condition might
     result.
3.        How does this strategy avoid       Organism        destruction by the complement?
          Disease
 Group A streptococci          No C5–C9                                 Streptococcal sore throat

 Haemophilus influenzae        Hides LPS, which can                     Meningitis
 type b                        activate C

 Pseudomonas aeruginosa        Binds C in solution instead              Septicemia; pyelonephritis
                               of on cell surface

 Trypanosoma cruzi             C5–C9 doesn’t get activated              Chagas’ disease

4.   Microorganisms       Effect Disease
 Influenzavirus                Kills host cell                          Influenza

 M. tuberculosis               Prevents digestion in phagocytes         Tuberculosis

 T. gondii                     Prevents digestion in phagocytes         Toxoplasmosis
 Trichophyton                     Digests keratin                        Athlete’s foot

 T. cruzi                         Prevents digestion in phagocytes       Chagas’ disease



Clinical Applications
1.   Kinins cause vasodilation and increased permeability of blood vessels. Symptoms should
     include increased secretions from the nose and eyes. Rhinoviruses cause the common cold.
2.   The proportions of white blood cells may change during diseases. The results of a differential
     count can be used to diagnose diseases. A patient with mononucleosis will have an increased
     number of monocytes. Neutropenia: decreased neutrophils. Eosinophilia: increased
     eosinophils.
3.   Phagocytosis is inhibited.
4.   Neutrophils will not phagocytize and they will die prematurely.
5.   a.   Mannose-binding lectin binds with mannose on the surface of a broad range of
          microorganisms. However, the mannose recognition pattern is not normally exposed on
          human cells.
     b.   Mannose-binding lectin deficiency results in increased susceptibility to infections in
          immunocompromised individuals and in young children.


Case History: Complement Evasion
The Problem
If a microbe is to be a successful parasite, it must avoid destruction by the host’s complement
system. The following list provides examples of known complement-evading techniques.
Complete the table to identify the disease and method of action.
                                                                  How does this strategy avoid
 Organism           Strategy                          Disease     destruction by the complement?

 Legionella         Uses C3b receptors to
 pneumophila        enter monocytes

 Pseudomonas        Produces proteases
 aeruginosa

 Salmonella         Activates C3 on long-chain
 enterica           LPS molecules

 Schistosoma        Sheds glycocalyx molecules
 mansoni



The Solution
                                      How does this strategy avoid destruction
 Organism                             by the complement?

 Legionella pneumophila               Binds cells instead of C3

 Pseudomonas aeruginosa               Degrades complement

 Salmonella enterica                  C5–C9 complex is too far away from cell surface to
                      cause damage

Schistosoma mansoni   Binds C in solution instead of on cell surface

								
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