Chapter 13 Nonspecific Defenses of the Host

SusceptibilityLack of resistance to a disease Resistance Ability to ward off disease Nonspecific resistanceDefenses against any pathogen Specific resistanceImmunity, 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 ( ) 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 Neutrophils60-70% Basophils0.5-1% Eosinophils2-4% Monocytes3-8% Lymphocytes20-25%

Neutrophils: Neutrophils Basophils: Produce Eosinophils: Toxic to parasites (i.e. helminths), some phagocytosis Monocytes: Phagocytic as mature macrophages 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

Redness Pain Heat Swelling (edema)

Chemicals Released by Damaged Cells HistamineVasodilation, increased permeability of blood vessels KininsVasodilation, increased permeability of blood vessels ProstaglandinsIntensify histamine and kinin effect LeukotrienesIncreased 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 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)

Figure 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.