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Chemicals Released by Damaged Cells

Chemicals Released by Damaged Cells. Inflammation. Figure 16.8a–b. Inflammation. Figure 16.8c–d. Fever: Abnormally High Body Temperature. Hypothalamus normally set at 37°C. Gram-negative endotoxin cause phagocytes to release interleukin–1 (IL–1).

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Chemicals Released by Damaged Cells

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  1. Chemicals Released by Damaged Cells

  2. Inflammation Figure 16.8a–b

  3. Inflammation Figure 16.8c–d

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

  5. Advantages Increase transferrins Increase IL–1 activity Disadvantages Tachycardia Acidosis Dehydration Fever

  6. The Complement System • Serum proteins activated in a cascade. Figure 16.9

  7. Effects of Complement Activation • Opsonization or immune adherence: Enhanced phagocytosis. • Membrane attack complex: Cytolysis. • Attract phagocytes. Figure 16.10

  8. Effects of Complement Activation Figure 16.11

  9. Classical Pathway Figure 16.12

  10. Alternative Pathway Figure 16.13

  11. Lectin Pathway Figure 16.14

  12. Some Bacteria Evade Complement • Capsules prevent C activation. • Surface lipid-carbohydrates prevent MAC formation. • Enzymatic digestion of C5a.

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

  14. Interferons (IFNs) Figure 16.15

  15. Transferrins Bind serum iron Antimicrobial peptides Lyse bacterial cells Innate Immunity

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