Innate Immune System Notes

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Innate Immunity: Nonspecific Defenses of the Host

Learning Objectives	Check Your Understanding
16-1    Differentiate innate and adaptive immunity.	Which defense system, innate or adaptive immunity, prevents entry of microbes into the body?
16-2    Define Toll-like receptors .	What relationship do Toll-like receptors have to pathogen-associated molecular patterns?
16-3    Describe the role of the skin and mucous membranes in innate immunity.	Identify one physical factor and one chemical factor that prevent microbes from entering the body through skin and mucous membranes.
16-4    Differentiate physical from chemical factors, and list five examples of each.	Identify one physical factor and one chemical factor that prevent microbes from entering or colonizing the body through the eyes, digestive tract, and respiratory tract.
16-5    Describe the role of normal microbiota in innate immunity.	Distinguish microbial antagonism from commensalism.
16-6    Classify leukocytes, and describe the roles of granulocytes and monocytes.	Compare the structures and function of monocytes and neutrophils.
16-7     Describe the six different types of white blood cells, and name a function for each type.	Define differential white blood cell count.
16-8    Differentiate the lymphatic and blood circulatory systems.	What is the function of lymph nodes?
16-9    Define phagocyte and phagocytosis .	What do fixed and wandering macrophages do?
16-10  Describe the process of phagocytosis, and include the stages of adherence and ingestion.	What is the role of TLRs in phagocytosis?
16-11  Identify six mechanisms of avoiding destruction by phagocytosis.	How does each of these bacteria avoid destruction by phagocytes? Streptococcus pneumoniae , Staphylococcus aureus , Listeria monocytogenes , Mycobacterium tuberculosis , Rickettsia
16-12  List the stages of inflammation.	What purposes does inflammation serve?
16-13  Describe the roles of vasodilation, kinins, prostaglandins, and leukotrienes in inflammation.	What causes the redness, swelling, and pain associated with inflammation?
16-14  Describe phagocyte migration.	What is margination?
16-15  Describe the cause and effects of fever.	Why does a chill indicate that a fever is about to occur?
16-16  List the major components of the complement system.	What is complement?
16-17  Describe three pathways of activating complement.	List the steps of complementation activation via (1) the classical pathway, (2) the alternative pathway, and (3) the lectin pathway.
16-18  Describe three consequences of complement activation.	Summarize the major outcomes of complement activation.
16-19  Define interferons.	What is interferon?
16-20  Compare and contrast the actions of IFN-α and IFN-β with IFN-γ.	Why do IFN-α and IFN-β share the same receptor on target cells, yet IFN-γ has a different receptor?
16-21  Describe the role of iron-binding proteins in innate immunity.	What is the role of siderophores in infection?
16-22  Describe the role of antimicrobial peptides in innate immunity.	Why are scientists interested in AMPs?

 

Chapter Summary

Introduction (p. 439)

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. 442)

ASM 3.4: The growth of microorganisms can be controlled by physical, chemical, mechanical, and biological means.

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 in plasma membranes of macrophages and dendritic cells bind to invading microbes.

   

First Line of Defense: Skin and Mucous Membranes (pp. 442–445)

1. The body’s first line of defense against infections is a physical barrier and the nonspecific chemicals of the skin and mucous membranes.

Physical Factors (pp. 442–444)

1. The structure of intact skin and the waterproof protein keratin provide resistance to microbial invasion.
2. Some pathogens 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. 444–445)

1. Fatty acids in sebum and earwax inhibit the growth of pathogenic bacteria.
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 (p. 445)

ASM 5.3: Microorganisms and their environment interact with and modify each other.

ASM 5.4: Microorganisms, cellular and viral, can interact with both human and non-human hosts in beneficial, neutral, or detrimental ways.

1. Normal microbiota change the environment, a process that can prevent the growth of pathogens.

Second Line of Defense (pp. 445–454)

1. A microbe’s penetration of the first line of defense encourages production of phagocytes, inflammation, fever, and antimicrobial substances.

Formed Elements in Blood (pp. 446–448)

1. Blood consists of plasma (fluid) and formed elements (cells and cell fragments).
2. Leukocytes (white blood cells) are divided into granulocytes (neutrophils, basophils, eosinophils) and agranulocytes.
3. During many infections, the number of leukocytes increases (leukocytosis); some infections are characterized by leucopenia (decrease in leukocytes).

White Blood Cells Links to an external site. 

The Lymphatic System (pp. 448–449)

1. The lymphatic system consists of lymph vessels, lymph nodes, and lymphoid tissue.
2. Interstitial fluid is returned to blood plasma via lymph vessels.

Phagocytes (pp. 449–452)

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. 449–450)

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 (pp. 450–451)

7. Chemotaxis is the process by which phagocytes are attracted to microorganisms.
8. Toll-like receptors on a phagocyte adhere 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 phagosome to complete ingestion.
10. Many phagocytized microorganisms are killed by lysosomal enzymes and oxidizing agents.

Microbial Evasion of Phagocytosis (p. 451)

ASM 2.3: Bacteria and Archaea have specialized structures (e.g., flagella, endospores, and pili) that often confer critical capabilities.

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.

Inflammation (pp. 452–453)

1. Inflammation is a bodily response to cell damage; it is characterized by redness, pain, heat, swelling, and sometimes the loss of function.
2. TNF-α stimulates production of acute-phase proteins.

   

Vasodilation and Increased Permeability of Blood Vessels (pp. 453–454)

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. 454–455)

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 (diapedesis).
7. Pus is the accumulation of damaged tissue and dead microbes, granulocytes, and macrophages.

    

Tissue Repair (p. 455)

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.

Fever (pp. 455–456)

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

Antimicrobial Substances (pp. 456–464)

The Complement System (pp. 456–460)

1. The complement system consists of a group of serum proteins that activate one another to destroy invading microorganisms.
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.

Interferons (pp. 460–461)

8. IFN-α and IFN-β are antiviral proteins produced in response to viral infection.
9. The mode of action of IFN-α and IFN-β is to induce uninfected cells to produce antiviral proteins (AVPs) that prevent viral replication.
10. IFN-α and IFN-β are host-cell-specific but not virus-specific.
11. IFN-γ activates neutrophils and macrophages to kill bacteria.

Iron-Binding Proteins (pp. 461–462)

12. Iron-binding proteins transport and store iron and deprive most pathogens of the available iron.

Antimicrobial Peptides (pp. 462–464)

13. Antimicrobial peptides (AMPs) inhibit cell wall synthesis; form pores in plasma membranes, resulting in lysis; and destroy DNA and RNA.
14. Antimicrobial peptides are produced by nearly all plants and animals, and bacterial resistance to AMPs has not yet been seen.