Inflammation & Immunity — Quick Reference

Innate vs Adaptive Immunity

  • Innate Immunity: First line, nonspecific, immediate defense; no memory.

  • Adaptive Immunity: Third line, specific targeting, develops memory.

  • Components:

    • Innate: Barriers, mast cells, granulocytes (neutrophils, eosinophils, basophils), monocytes/macrophages, NK cells, platelets, endothelial cells.

    • Adaptive: T/B lymphocytes, dendritic cells, macrophages (antigen presentation).

  • Common features: Complement, clotting, kinins activate both; phagocytosis shared.

  • Memory: Adaptive has memory; innate does not.

Inflammatory Response: Overview

  • Second line, nonspecific, rapid activation in vascularized tissue.

  • Aims: Limit damage, destroy microbes, initiate healing, activate adaptive immunity.

  • Can be local or systemic.

First-Line Defenses (Barriers)

  • Physical/Mechanical: Skin, epithelial sloughing, mucosal barriers (secretions, cilia).

  • Chemical: Lysozyme, acidic gastric secretions, normal flora.

  • Other: Rapid mechanical clearance, tight junctions.

Second-Line Defenses: Inflammation

  • Innate, nonspecific response at injury/infection site.

  • Rapid vascular and cellular responses to contain damage and begin repair.

  • Primes adaptive immunity.

Acute Inflammation: Key Events

  • Triggers: Tissue injury or pathogen invasion.

  • Vascular changes: Vasodilation (erythema, warmth); increased permeability (edema).

  • Mast cell activation: Degranulation (histamine, PAF, chemotactic factors) and new mediator synthesis (prostaglandins, leukotrienes).

  • Plasma protein cascades: Complement, clotting, kinins activated.

  • Cellular events: Chemotaxis, leukocyte infiltration, phagocytosis (pus).

  • Mediators: TNF-α, interleukins, interferons; growth factors; hemostasis; pain.

Mast Cells: Degranulation and Synthesis

  • Degranulation releases: Histamine, chemotactic factors, cytokines, PAF.

  • Synthesis releases: Arachidonic acid metabolites (prostaglandins, leukotrienes), growth factors.

  • Net effects: Vasodilation, increased permeability, leukocyte chemotaxis, pain, mediator production.

Plasma Protein Systems

  • Complement: Opsonization (C3b), anaphylatoxins (C3a, C5a), MAC (C5b-9) via classical, lectin, alternative pathways.

  • Clotting: Forms fibrin barrier, interacts with inflammation.

  • Kinins: Bradykinin; increases permeability, vasodilation, pain.

  • Overall: Amplifies and orchestrates inflammation.

Vascular Stage of Inflammation

  1. Brief vasoconstriction.

  2. Vasodilation (NO, histamine) →\rightarrow increased blood flow.

  3. Increased permeability →\rightarrow exudate, edema.

  4. Leukocyte adhesion (margination).

  5. Leukocyte emigration (diapedesis) into tissue.

  6. Chemotaxis →\rightarrow recruitment of neutrophils, monocytes.

Cellular Stage: Neutrophils

  • Adhere, transmigrate (diapedesis), chemotaxis.

  • Phagocytosis and microbial killing; short-lived in acute inflammation.

Cellular Stage: Monocytes/Macrophages

  • Monocytes migrate in, differentiate into macrophages.

  • Phagocytosis improved by opsonization (Ab, C3b).

  • Antigen presentation activates T cells.

Local and Systemic Effects of Inflammation

  • Local: Leukocyte recruitment, chemotaxis, phagocytosis, tissue repair.

  • Systemic: Fever, leukocytosis, elevated acute-phase proteins (CRP, fibrinogen, SAA).

  • Cytokines: Proinflammatory (TNF-α, IL-1, IL-6, IFN-γ) and anti-inflammatory (IL-10) signals govern resolution.

Acute vs Chronic Inflammation

  • Acute: Rapid, self-limited (if successful), resolves/heals.

  • Chronic: Persistent injury/infection; ongoing inflammation and repair.

  • Transition: Granulomatous or non-granulomatous proliferative chronic inflammation.

Chronic Inflammation: Features

  • Persistent macrophage/lymphocyte activation; fibroblast recruitment.

  • Granulomatous chronic inflammation is possible (Langhans-type giant cells).

  • Fibrosis and scar formation during repair.

Granulocytes Overview

  • Neutrophils: Primary phagocytes in acute bacterial infection.

  • Eosinophils: Kill parasitic worms; modulate allergy/asthma.

  • Basophils: Release histamine and inflammatory mediators.

  • Key: Neutrophils dominate acute; eosinophils/basophils in allergic/parasitic responses.