Chapter 13

Nonspecific Defenses of the Host

• Susceptibility Lack of resistance to a disease

• Resistance Ability to ward off disease

• Nonspecific resistance Defenses against any pathogen

• Specific resistance Immunity, resistance to a specific pathogen

TERMS

Host Defenses

Figure 16.1

• Skin

• Epidermis: tightly packed cells with outer layer of dead cells with keratin, a protective protein

• Sloughing off dead cells

• Dry environment

Mechanical Factors

• Mucous membranes

• Microbes trapped in mucus are transported away from the lungs

• Washes eye

• Saliva: Washes microbes off

• Urine: Flows out

• Vaginal secretions: Flow out

Mechanical Factors

• Bacteriostatic and fungistatic fatty acid in sebum

• Low pH (3-5) of skin

• in perspiration, tears, saliva, and tissue fluids

• Low pH (1.2-3.0) of gastric juice

• in blood bind iron

Chemical Factors

• Microbial antagonism/competitive exclusion: Normal microbiota compete with pathogens.

• nutrients

• antimicrobials

Normal Microbiota

• Percentage of each type of white blood cell in the WBC population.

Differential White Cell Count

Neutrophils 60-70%

Basophils 0.5-1%

Eosinophils 2-4%

Monocytes 3-8%

Lymphocytes 20-25%

• Neutrophils:

• Basophils: Produce

• Eosinophils: Toxic to parasites (i.e. helminths), some phagocytosis

• Monocytes: Phagocytic as mature macrophages

White Blood Cells

White Blood Cells• are found in various

tissues such as the liver, lungs and nervous tissue

• roam tissues

• Involved in specific immunity

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Phagocytosis

Figure 16.8a

• Caused by immune system participants

• Vasodilation

• Margination and emigration of WBCs

• Acute-phase proteins activated (complement, cytokine, vasodilators)

Inflammation

Inflammation• Redness

• Pain

• Heat

• Swelling (edema)

Chemicals Released by Damaged Cells

• Histamine Vasodilation, increased permeability of blood vessels

• Kinins Vasodilation, increased permeability of blood vessels

• Prostaglandins Intensify histamine and kinin effect

• Leukotrienes Increased permeability of blood vessels, phagocytic attachment

Inflammation

Figure 16.9a, b

Inflammation

Figure 16.9c, d

• Serum proteins activated in a cascade.

• C3a

• C3b

• C5a

• C5b, C6, C7, C8, C9

The Complement System

Figure 16.10

Effects of Complement Activation• Membrane attack

complex: cytolysis

• Opsonization: enhanced phagocytosis

Figure 16.11

Cytolysis via complement activation

Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Effects of Complement Activation• Inflammation: and attraction of

phagocytes via

vasodilation Chemotaxis

Classical Pathway

Figure 16.13

Alternative Pathway

Figure 16.14

Lectin Pathway

Figure 16.15

Some bacteria evade complement• may prevent complement activation

• Capsule lipid-carbohydrates may prevent MAC formation and

• Enzymatic digestion of C5a (inhibits inflammation and chemotaxis)

• Alpha IFN & Beta IFN

• Cause cells to produce antiviral proteins that inhibit viral replication

• Gamma IFN

• Causes neutrophils and macrophages to phagocytize bacteria

Interferons (IFNs)

Interferons (IFNs)

Figure 16.16

1

2

3

4

5

Viral RNA from an infecting virus enters the cell.

The infecting virus replicates into new viruses.

The infecting virus also induces the host cell to produce alpha and beta interferons.

Interferons released by the virus-infected host cell bind to plasma membrane or nuclear membrane receptors on uninfected neighboring host cells, inducing them to synthesize antiviral proteins (AVPs).

New viruses released by the virus-infected host cell infect neighboring host cells. 6 AVPs degrade viral

m-RNA and inhibit protein synthesis and thus interfere with viral replication.