Inflammation is the protective response of living tissues to any form of injury. Its goal is to remove the harmful agent, clear dead tissue and start healing. Inflammation is local, but in some cases it becomes widespread and causes systemic inflammatory response or sepsis.
Inflammation is not the same as infection. Infection is caused by microorganisms, while inflammation is the body’s response to injury of any kind.
Etiology of Inflammation
Common agents that trigger inflammation include:
- Physical agents: Heat, cold, radiation, trauma
- Chemical agents: Organic and inorganic poisons
- Infective agents: Bacteria, viruses and toxins
- Immunological causes: Antigen–antibody reactions, cell-mediated immunity
Cardinal Signs of Inflammation
The classical five signs are:
- Redness (Rubor): Due to increased blood flow
- Swelling (Tumor): Due to fluid accumulation
- Heat (Calor): More blood reaching the affected area
- Pain (Dolor): Chemical mediators stimulate nerve endings
- Loss of function (Functio laesa): Later added by Virchow
Types of Inflammation
1. Acute Inflammation
Short-lasting response that appears quickly after an injury. Examples: acute bronchitis, sore throat, skin cuts, appendicitis, tonsillitis, meningitis.
2. Chronic Inflammation
Long-standing inflammation due to persistent injury or slow-acting stimuli. Examples: asthma, tuberculosis, rheumatoid arthritis, chronic sinusitis, ulcerative colitis.
Pathogenesis of Acute Inflammation
The events of acute inflammation are divided into:
- I) Vascular events
- II) Cellular events
I. Vascular Events
These occur in the microcirculation (arterioles, capillaries, venules) and include hemodynamic changes and increased vascular permeability.
a) Hemodynamic Changes
The sequence includes:
- Transient vasoconstriction: Immediate response lasting seconds to minutes.
- Vasodilatation: Mainly of arterioles → increases blood flow → causes redness and heat.
- Increased hydrostatic pressure: Leads to transudation of fluid → localized swelling.
- Slowing of blood flow (stasis): Due to fluid loss and increased viscosity.
- Margination of leukocytes: Neutrophils move towards vessel walls and begin exiting the vessel.
Lewis’ Triple Response demonstrates vascular changes:
- Red line: Local vasodilatation
- Flare: Dilatation of surrounding arterioles
- Wheal: Local swelling due to fluid leakage
b) Increased Vascular Permeability
Normally, endothelial cells form a tight barrier. During inflammation, they become leaky due to:
- Endothelial cell contraction: Most common; mediated by histamine, bradykinin; rapid and short-lived.
- Cytoskeletal retraction: Slower response mediated by IL-1 and TNF-α; lasts longer.
- Direct endothelial injury: Causes necrosis and gaps; due to burns, toxins.
- Leukocyte-mediated injury: Activated neutrophils release toxic substances damaging endothelium.
- Leaky new vessels: Newly formed capillaries during repair are naturally permeable.
II. Cellular Events
These involve movement of leukocytes from the blood to the site of injury and their activation.
a) Exudation and Migration of Leukocytes
The sequence is:
1. Margination
Due to stasis, neutrophils move from the center of the vessel to the periphery.
2. Rolling
Leukocytes loosely roll along the endothelium through weak bonds mediated by selectins.
3. Adhesion
Firm binding occurs between leukocytes and endothelial cells using adhesion molecules like integrins, ICAM-1, VCAM-1.
4. Transmigration (Diapedesis)
Leukocytes squeeze through endothelial gaps using pseudopods and enzymes like collagenase.
5. Chemotaxis
Leukocytes migrate towards the site of injury following chemical gradients. Chemotactic agents include bacterial products, IL-8, fibrin, complement fragments and MCP-1.
b) Phagocytosis
Phagocytosis is the process where neutrophils and macrophages engulf and destroy microbes and debris.
Steps include:
- Recognition and attachment of particles
- Engulfment into a phagosome
- Killing and digestion by lysosomal enzymes such as lysozyme, proteases, collagenase and elastase
Detailed Notes:
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