Cellular components of inflammation

Neutrophils - First Responder Firefight

• Primary Role: Acute inflammation's first responders, arriving in 6-24 hours.

• Key Features: Multi-lobed nucleus, granular cytoplasm. Phagocytose, degranulate, and release Neutrophil Extracellular Traps (NETs).

• Recruitment: Follows a specific sequence:

• Chemotaxis: Migrate toward specific signals. 📌 Mnemonic: CILK - C5a, IL-8, LTB4, Kallikrein.

• Killing: Use phagocytosis and respiratory burst ($O_2 ightarrow O_2^{\cdot-}$ via NADPH oxidase).

⭐ Leukocyte Adhesion Deficiency (LAD): Defect in integrins (CD18) impairs adhesion. Presents with delayed umbilical cord separation, recurrent bacterial infections, and neutrophilia without pus formation.

Macrophages - Clean-up & Command

• Arrival: Monocytes migrate from blood, becoming macrophages in tissue 24-48 hours post-injury, succeeding neutrophils.
• Core Functions:
  • Phagocytosis: Engulf cellular debris, pathogens, and dead neutrophils.
  • Antigen Presentation: Process and present antigens to helper T-cells, linking innate and adaptive immunity.
  • Orchestration: Secrete cytokines (TNF, IL-1, IL-6) to manage inflammation and initiate healing.
• Activation Pathways:
  • M1 (Classical): Pro-inflammatory; activated by IFN-γ. Destroys microbes.
  • M2 (Alternative): Anti-inflammatory; activated by IL-4, IL-13. Drives tissue repair and fibrosis.

⭐ In granulomatous inflammation (e.g., Tuberculosis), macrophages transform into epithelioid cells and can fuse to form multinucleated giant cells.

Leukocyte Extravasation - The Great Escape

The sequential process of leukocytes exiting the vasculature to reach tissues. It's a critical component of acute inflammation, guided by specific adhesion molecules and chemokines.

📌 Mnemonic: "Rolling, Adhesion, Diapedesis, Migration"

• Rolling: Mediated by low-affinity selectin binding.
• Adhesion: Firm attachment via high-affinity integrins.
• Transmigration: Squeezing between endothelial cells.
• Migration: Movement along a chemotactic gradient.

⭐ Leukocyte Adhesion Deficiency (LAD-1): An autosomal recessive defect in the CD18 subunit of integrins. Presents with recurrent bacterial infections without pus, poor wound healing, delayed umbilical cord separation, and marked neutrophilia.

Other Cells - Specialized Forces

• Mast Cells & Basophils:

  • Sentinel cells in connective tissue; activated by IgE, C3a/C5a, trauma.
  • Release preformed histamine granules → vasodilation & ↑ vascular permeability.
  • Central to Type I hypersensitivity reactions.

• Eosinophils:

  • Combat helminthic parasites and modulate allergic reactions.
  • Granules contain Major Basic Protein (MBP), toxic to parasites.

• Lymphocytes & Plasma Cells:

  • Key drivers of chronic inflammation and the adaptive immune response.

⭐ Eosinophil granules contain crystalloid bodies, which can form Charcot-Leyden crystals, a classic finding in asthmatic sputum.

High‑Yield Points - ⚡ Biggest Takeaways

• Neutrophils are the first responders in acute inflammation, phagocytosing bacteria.
• Macrophages arrive in 24-48 hours, driving chronic inflammation and presenting antigens.
• Lymphocytes (T & B cells) are hallmarks of chronic inflammation and adaptive immunity.
• Eosinophils are characteristic of allergic reactions and parasitic infections.
• Mast cells and basophils release histamine, mediating vasodilation and increased permeability.
• Giant cells are fused macrophages, pathognomonic for granulomatous inflammation.