1. Nonspecific Defenses of the Host
Chapter 16
Nonspecific Defenses of the Host

2. 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

3. Host Defenses
Figure 16.1

4. Mechanical Factors Skin
Epidermis consists of tightly packed cells with
Keratin, a protective protein

5. Mechanical Factors Mucous membranes
Ciliary escalator: Microbes trapped in mucus are transported away from the lungs
Lacrimal apparatus: Washes eye
Saliva: Washes microbes off
Urine: Flows out
Vaginal secretions: Flow out

6. Chemical Factors Fungistatic fatty acid in sebum Low pH (3-5) of skin
Lysozyme in perspiration, tears, saliva, and tissue fluids
Low pH ( ) of gastric juice
Transferrins in blood find iron
NO inhibits ATP production

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

8. Formed Elements In Blood
Table 16.1

9. Differential White Cell Count
Percentage of each type of white cell in a sample of 100 white blood cells
Neutrophils
60-70%
Basophils
0.5-1%
Eosinophils
2-4%
Monocytes
3-8%
Lymphocytes
20-25%

10. White Blood Cells Neutrophils: Phagocytic Basophils: Produce histamine
Eosinophils: Toxic to parasites, some phagocytosis
Monocytes: Phagocytic as mature macrophages
Fixed macrophages in lungs, liver, bronchi
Wandering macrophages roam tissues
Lymphocytes: Involved in specific immunity

11. Phagocytosis Phago: eat Cyte: cell
Ingestion of microbes or particles by a cell, performed by phagocytes

12. Phagocytosis
Figure 16.8a

13. Microbial Evasion of Phagocytosis
• Inhibit adherence: M protein, capsules
Streptococcus pyogenes, S. pneumoniae
• Kill phagocytes: Leukocidins
Staphylococcus aureus
• Lyse phagocytes: Membrane attack complex
Listeriamonocytogenes
• Escape phagosome
Shigella
• Prevent phagosome-lysosome fusion
HIV
• Survive in phagolysosome
Coxiella burnetti

14. Inflammation Redness Pain Heat Swelling (edema)
Acute-phase proteins activated (complement, cytokine, kinins)
Vasodilation (histamine, kinins, prostaglandins, leukotrienes)
Margination and emigration of WBCs
Tissue repair

15. Chemicals Released by Damaged Cells
• Histamine
Vasodilation, increased permeability of blood vessels
• Kinins
• Prostaglandins
Intensity histamine and kinin effect
• Leukotrienes
Increased permeability of blood vessels, phagocytic attachment

16. Inflammation
Figure 16.9a, b

17. Inflammation
Figure 16.9c, d

18. Fever: Abnormally High Body Temperature
Hypothalamus normally set at 37°C
Gram-negative endotoxin cause phagocytes to release interleukin 1
Hypothalamus releases prostaglandins that reset the hypothalamus to a high temperature
Body increases rate of metabolism and shivering to raise temperature
When IL-1 is eliminated, body temperature falls. (Crisis)

19. The Complement System Serum proteins activated in a cascade.
Figure 16.10

20. Effects of Complement Activation
Opsonization or immune adherence: enhanced phagocytosis
Membrane attack complex: cytolysis
Attract phagocytes
Figure 16.11

21. Effects of Complement Activation
Figure 16.12

22. Classical Pathway
Figure 16.13

23. Alternative Pathway
Figure 16.14

24. Lectin Pathway
Figure 16.15

25. Some bacteria evade complement
Capsules prevent C activation
Surface lipid-carbohydrates prevent MAC formation
Enzymatic digestion of C5a

26. Interferons (IFNs)
Alpha IFN & Beta IFN: Cause cells to produce antiviral proteins that inhibit viral replication
Gamma IFN: Causes neutrophils and macrophages to phagocytize bacteria

27. Interferons (IFNs) 2
The infecting virus replicates into new viruses. 5
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. 1
Viral RNA from an infecting virus enters the cell. 3
The infecting virus also induces the host cell to produce interferon on RNA (IFN-mRNA), which is translated into alpha and beta interferons. 4
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). These include oligoadenylate synthetase, and protein kinase.
Figure 16.16