25. Acute inflammation - classification, etiology, pathogenesis.

Acute inflammation - classification, etiology, pathogenesis.

Acute inflammation is the immediate, early response of vascularized tissues to injury or infection, aimed at eliminating the cause and initiating repair.

Duration: Short (minutes to days).

Main cells involved: Neutrophils (first responders).

Classification of Acute Inflammation

Based on type of exudate

Etiology (Causes)

1. 1 Infectious agents

Bacteria, viruses, fungi, parasites.

Example: Streptococcus pyogenes → sore throat (pharyngitis).

1. 2 Physical agents

Trauma, burns, frostbite, radiation.

1. 3 Chemical agents

Toxins, acids, alkalis.

1. 4 Foreign bodies

Splinters, dirt, surgical sutures.

1. 5 Immunologic reactions (hypersensitivity)

Allergic reactions, autoimmune diseases.

Pathogenesis of Acute Inflammation

1. 1 Recognition of injury/ infection

Resident immune cells (macrophages, mast cells, dendritic cells) recognize:

• PAMPs (pathogen- associated molecular patterns).
• DAMPs (damage- associated molecular patterns).

Activation of Toll-like receptors (TLRs) and inflammasomes.

1. 2 Vascular phase

Vasodilation → increased blood flow (rubor, calor ).

• Mediators: Histamine, Prostaglandins.

Increased vascular permeability → exudation of plasma proteins and leukocytes ( tumor ).

• Mediators: Histamine, Bradykinin, Leukotrienes.

1. 3 Cellular phase

Leukocyte recruitment (primarily neutrophils):

1. Margination and rolling (selectins).
2. Adhesion (integrins).
3. Transmigration (diapedesis) across endothelium (PECAM- 1).
4. Chemotaxis: migration toward site via chemokines (IL- 8, C5a).

Phagocytosis:

1. Recognition: via opsonins (IgG, C3b).
2. Engulfment: phagosome + lysosome = phagolysosome.
3. Killing: ROS, NO, lysosomal enzymes.
4. 4 Termination of inflammation

Anti- inflammatory mediators begin to dominate:

• IL-10, TGF-β, lipoxins.

Clearance of neutrophils, resolution of exudate.

Systemic Responses (Acute- Phase Reaction)

Fever: IL- 1, TNF- α → PGE2 → hypothalamic temperature set point ↑ .

Leukocytosis: Especially neutrophilia in bacterial infections.

Acute-phase proteins:

• CRP, fibrinogen, serum amyloid A (produced by liver).

Tachycardia, anorexia, malaise: due to cytokines.

Outcomes of Acute Inflammation

1. Resolution: complete tissue repair (if injury is short- lived).
2. Healing by fibrosis: if tissue cannot regenerate or damage is extensive.
3. Progression to chronic inflammation: if stimulus persists or resolution fails.