Characteristics of acute inflammation (cellular events, chemical mediators, systemic effects, exudate, organic example)

1. Definition

Inflammation is a protective response that eliminates the initial cause of cell injury along with the necrotic cells/tissue produced by it, by delivering host-defense cells and molecules from the blood to the site of injury. Named with the organ + “-itis” (exception: pneumonia). It is either acute or chronic.

Acute inflammation: rapid onset, short duration; main cells neutrophils (and platelets). The five cardinal signs are rubor (redness), tumor (swelling), dolor (pain), calor (heat), and functio laesa (loss of function).

Stimuli: infections, trauma / physical-chemical agents (burns, irradiation), tissue necrosis (ischemia), foreign bodies, and immune/hypersensitivity reactions.

2. Recognition (innate immunity)

• Toll-like receptors (TLR) recognize pathogen-associated molecular patterns (PAMPs, e.g. LPS).
• Sensors of injury recognize damage-associated molecular patterns (DAMPs).
• Circulating proteins — complement, mannose-binding lectins, collectins.
• Functions: activate complement/coagulation/phagocytosis, trigger inflammatory cascades, induce apoptosis.

3. Vascular events

1. Transient vasoconstriction → vasodilation → ↑ blood flow (redness, warmth).
2. ↑ vascular permeability — endothelial contraction forms gaps: early via histamine, bradykinin (15–30 min), late via TNF, IL-1, IFN-γ (4–6 h, lasts ~24 h); also endothelial injury, leakage from new vessels, VEGF-driven transcytosis.
3. Consequences — protein-rich exudate leaves vessels → blood concentrates → ↑ viscosity → stasis; ↑ interstitial osmotic pressure → edema.

4. Cellular events — leukocyte recruitment

1. Margination & rolling — leukocytes pushed to vessel edge; weak adhesion via selectins (E-/P- on endothelium, L- on leukocytes).
2. Firm adhesion — integrins (chemokine-activated) bind ICAM/VCAM.
3. Transmigration / diapedesis — squeeze between endothelial cells (mostly venules) via CD31 (PECAM-1); collagenase breaches basement membrane.
4. Chemotaxis — toward bacterial products, chemokines, complement (C5a), arachidonic-acid products (LTB4).
5. Phagocytosis & killing — opsonization (IgG-Fc, C3b) → engulfment → ROS (oxidative burst), nitrogen species, lysosomal enzymes; NETs trap microbes.

5. Chemical mediators

Mediator	Source	Main actions
Histamine / serotonin	Mast cells, basophils, platelets	Vasodilation, ↑ permeability
Prostaglandins (PGE2)	COX pathway	Vasodilation, pain, fever
Leukotrienes	Lipoxygenase pathway	Chemotaxis, bronchospasm, ↑ permeability
TNF / IL-1 / IL-6	Macrophages, endothelium	Endothelial activation, acute-phase response
Complement (C3a, C5a)	Plasma (liver)	Anaphylatoxins, chemotaxis, MAC, opsonization
Bradykinin	Kinin system (factor XII)	↑ permeability, vasodilation, pain
NO	Endothelium, macrophages	Vasodilation, microbial killing
PAF	Membrane phospholipids	Platelet aggregation, vasoconstriction

Factor XII (Hageman) activation links the clotting, kinin, and fibrinolytic systems to inflammation.

6. Systemic effects (acute-phase reaction)

Driven mainly by TNF, IL-1, IL-6:

• Fever — exogenous pyrogens (LPS) → IL-1/TNF → ↑ COX → PGE2 raises the hypothalamic set point.
• ↑ acute-phase proteins — CRP, serum amyloid A, fibrinogen (opsonins; fibrinogen ↑ ESR).
• Leukocytosis — cytokines release marrow reserves; CSF in prolonged infection (some infections cause leukopenia).
• ↑ HR/BP; in overwhelming infection → septic shock (TNF/IL-1 → hypotension, DIC, acidosis, hypoglycemia).

7. Morphologic patterns (by exudate) & organ examples

Pattern	Exudate	Examples
Serous	Thin, low-protein (no fibrin/cells)	Burn blisters, effusions, common cold
Fibrinous	Fibrin-rich	“Hairy heart” pericarditis, pseudomembranous colitis (C. difficile), diphtheria
Purulent (suppurative)	Pus (PMNs + necrosis)	Abscess, empyema, phlegmon; furuncle/carbuncle
Hemorrhagic	RBC-rich (severe vascular damage)	Hemorrhagic pneumonia, anthrax, smallpox
Gangrenous	Necrosis + bacteria	Wet gangrene (DM, atherosclerosis), gas gangrene

Outcomes of acute inflammation: resolution, scarring/fibrosis (organization of unabsorbed exudate), or progression to chronic inflammation.

💡 High-yield: Cardinal signs (rubor, tumor, dolor, calor, functio laesa). Recruitment cascade: rolling (selectins) → adhesion (integrins–ICAM) → diapedesis (PECAM-1) → chemotaxis. Early permeability = histamine; late = TNF/IL-1. Acute-phase trio = TNF, IL-1, IL-6 → fever, CRP, leukocytosis. Exudate patterns: serous → fibrinous → purulent → hemorrhagic → gangrenous.