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Here is a full explanation of the content in your image, which covers Chemotaxis - a key step in acute inflammation.
Chemotaxis - Explained
Definition
Chemotaxis is the directed migration of leukocytes (white blood cells) toward an inflammatory stimulus, moving along a chemical concentration gradient of locally produced substances called chemoattractants.
Think of it like a GPS signal - the injured/infected tissue releases chemical "breadcrumbs," and leukocytes follow the trail toward the source.
Chemoattractants - What Attracts the Leukocytes?
These are chemicals produced by microbes, host cells, and during immune reactions. They are divided into:
Exogenous (from outside the body - microbes)
- N-formylmethionine peptides - bacterial products with a characteristic N-fMet terminus. Since human cells don't use fMet (only bacteria/mitochondria do), these are immediately recognized as "foreign."
Endogenous (produced by the host itself)
| Chemoattractant | Source | Notes |
|---|---|---|
| IL-8 (Interleukin-8 / CXCL8) | Chemokine family, secreted by macrophages & endothelium | Most important chemokine for neutrophil recruitment |
| C5a | Complement activation | Also increases vascular permeability |
| C3a | Complement activation | Also called anaphylatoxin |
| LTB4 (Leukotriene B4) | Arachidonic acid via the lipoxygenase pathway | Potent chemoattractant for neutrophils |
How Do Leukocytes Accumulate at the Site?
Once leukocytes are attracted, they physically anchor themselves by binding to extracellular matrix (ECM) proteins using two types of adhesion molecules:
- Integrins - transmembrane receptors that grip fibronectin, laminin, collagen in the ECM
- CD44 - a surface molecule that binds hyaluronic acid in the matrix
This ensures leukocytes don't just pass through - they stay put and do their job.
Sequence of Leukocyte Infiltration (Timing)
This is a classic exam fact:
| Time | Cell Type |
|---|---|
| 0-6 hours | Neutrophils begin arriving |
| 6-24 hours | Neutrophils predominate |
| 24-48 hours | Neutrophils are replaced by monocytes (which become macrophages in tissues) |
The reason for this switch: neutrophils are short-lived (they undergo apoptosis quickly), while monocytes/macrophages are more durable and take over for sustained inflammation and cleanup.
Right-Side Panel: Leukocyte Adhesion Deficiency (LAD)
The right side of the image appears to describe Leukocyte Adhesion Deficiency (LAD), a genetic immunodeficiency:
- Caused by mutations in integrin genes (specifically CD18, the beta-2 integrin subunit)
- Impaired integrin activation means leukocytes cannot bind to vessel walls or ECM
- Features: Recurrent infections, persistent leukocytosis (WBCs pile up in blood since they can't leave), Bombay blood group association, recurrent infections, delayed umbilical cord separation, mental retardation
- Selectin defects are also listed, pointing to another adhesion molecule failure
Clinical Importance
- These pathways are targets for anti-inflammatory drugs (e.g., steroids reduce chemokine production; biologics like anti-IL-8 antibodies)
- LTB4 pathway inhibition is relevant in asthma treatment (montelukast targets the related cysteinyl leukotrienes)
- Understanding LAD explains why patients with this condition cannot fight bacterial infections despite having normal or elevated WBC counts in the blood
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