Inflammation – An Easy Guide

🔹 What is Inflammation?

Inflammation is the body’s protective response to injury, infection, or irritation.
Its goal is simple:

1. Eliminate the cause of injury (like microbes or toxins).
2. Clear out damaged tissue.
3. Start repair.

It is not always harmful — it’s a survival mechanism. But when excessive or uncontrolled, inflammation itself can cause disease.

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🔹 The Classic Signs

Historically, inflammation is remembered by the five cardinal signs (from Roman medicine):

1. Redness (Rubor) – due to increased blood flow.
2. Heat (Calor) – also from increased blood flow and metabolism.
3. Swelling (Tumor) – fluid leakage into tissues.
4. Pain (Dolor) – chemical mediators stimulating nerves.
5. Loss of function (Functio laesa) – impaired movement or activity.

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🔹 Types of Inflammation

1. Acute Inflammation
   • Rapid, short-lived (minutes to days).
   • Dominated by neutrophils.
   • Aims at quick defense and repair.
2. Chronic Inflammation
   • Long-lasting (weeks to years).
   • Dominated by lymphocytes, macrophages, fibroblasts.
   • Leads to tissue damage and scarring (fibrosis).

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🔹 The Steps of Acute Inflammation (Simplified Timeline)

1. Vascular Changes
   • Injury/infection triggers release of chemicals (like histamine, nitric oxide).
   • Blood vessels dilate → more blood (redness, heat).
   • Vessel walls become leaky → plasma proteins and fluid enter tissues (swelling).
2. Cellular Events
   • Neutrophils are first responders.
   • They move from blood → tissue by a process called extravasation:
     • Margination → stick to vessel walls.
     • Rolling → interact weakly with endothelial cells.
     • Adhesion → firm attachment via integrins.
     • Transmigration → squeeze between endothelial cells into tissue.
3. Phagocytosis & Killing
   • Neutrophils and macrophages engulf bacteria/debris.
   • Use reactive oxygen species, nitric oxide, and enzymes to destroy invaders.
4. Resolution or Repair
   • If injury clears → healing begins.
   • If not → progresses to chronic inflammation.

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🔹 Chemical Mediators of Inflammation

Inflammation is basically a chemical orchestra. Key mediators include:

• Histamine → from mast cells; increases vascular permeability.
• Prostaglandins → cause fever, pain, vasodilation.
• Leukotrienes → attract white blood cells.
• Cytokines (IL-1, TNF-α, IL-6) → coordinate the whole response, cause fever.
• Complement system proteins → punch holes in microbes, attract immune cells.

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🔹 Anatomy Behind It

• Blood vessels → the main stage for vascular changes.
• Endothelial cells → control entry of immune cells.
• Connective tissue → where fluid and immune cells accumulate.
• Local nerves → transmit pain signals when irritated by mediators.

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🔹 Biochemistry Behind It

• Arachidonic Acid Pathway (from cell membranes):
  • Cyclooxygenase (COX) → Prostaglandins, Thromboxanes.
  • Lipoxygenase → Leukotrienes.
  • These products explain why NSAIDs (like ibuprofen) work — they block COX, reducing prostaglandins → less pain, swelling, fever.
• Reactive Oxygen Species (ROS): Used by neutrophils to kill microbes.
• Nitric Oxide: Vasodilator and antimicrobial.

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🔹 Chronic Inflammation

When the cause is not eliminated, or in autoimmune diseases, acute inflammation transitions to chronic.

• Cells involved: Lymphocytes (T, B cells), macrophages, plasma cells.
• Features: Continuous tissue destruction, attempts at repair (fibrosis, angiogenesis).
• Examples: Tuberculosis, rheumatoid arthritis, chronic hepatitis.

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🔹 Clinical Relevance

• Pneumonia: Acute inflammation in the lungs.
• Asthma: Chronic airway inflammation.
• Atherosclerosis: Chronic inflammation of arterial walls.
• Autoimmune diseases: Inappropriate inflammation against self-tissues.
• Anti-inflammatory drugs:
  • Steroids → suppress cytokines, broad anti-inflammatory effect.
  • NSAIDs → block prostaglandins, relieve pain and fever.
  • Biologics (like anti-TNF drugs) → target specific cytokines.

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🔹 Summary for Students

Inflammation is the body’s first line of organized defense when tissues are injured.

• Acute: Fast, neutrophil-driven, short-term.
• Chronic: Slow, lymphocyte/macrophage-driven, long-term, tissue damage.
• Mediators: Histamine, prostaglandins, cytokines, complement.
• Purpose: Eliminate cause, clear debris, repair tissue.

👉 Think of inflammation as a firefighting team:

• Fire trucks rush in (neutrophils).
• Hoses spray water everywhere (fluid leakage).
• Commanders give orders (cytokines).
• If the fire is controlled → clean-up and rebuilding (healing).
• If not → smoldering fire that damages the house itself (chronic inflammation).

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Mnemonic to Remember:
“Inflammation = Red, Hot, Swollen, Painful, and Lost.”