General pathology · Inflammation
Leukocyte recruitment: rolling, adhesion, transmigration, chemotaxis !
- Process
White cells leave the blood in steps: they roll on the vessel wall, stick firmly, squeeze between endothelial cells and crawl toward the injury.
Updated 2026-11-01
What it is
Leukocytes reach injured tissue through a multistep cascade, mostly in postcapillary venules. Selectins slow them down, chemokines switch their integrins to a high-affinity state, integrins anchor them, and PECAM-1 helps them cross the endothelium; then they follow chemical gradients. Each step has an inherited defect, which makes this a favourite exam topic.
Key facts
- Neutrophils arrive first (6–24 hours): they are abundant, respond fast to chemokines and bind E- and P-selectin well; monocytes follow at 24–48 hours and live longer.
- Exceptions: Pseudomonas infections keep recruiting neutrophils for days; viral infections draw lymphocytes first; allergy and parasites draw eosinophils.
- L-selectin is on the leukocyte; E- and P-selectin are on the endothelium (P-selectin is stored in Weibel-Palade bodies and also found on platelets).
- Recruitment happens mainly in postcapillary venules; in the lung neutrophils also leave through capillaries.
Step by step
- Margination: slow flow in dilated venules pushes leukocytes from the centre of the stream to the vessel wall.
- Rolling: endothelial E- and P-selectin, induced by TNF, IL-1 and histamine, bind sialyl-Lewis X on leukocytes in weak, quick bonds.
- Activation: chemokines such as IL-8 (CXCL8) displayed on endothelium switch leukocyte integrins to a high-affinity shape.
- Firm adhesion: β2 integrins (LFA-1, Mac-1) bind ICAM-1 and VLA-4 binds VCAM-1, and the cell stops.
- Transmigration (diapedesis): the cell squeezes between endothelial cells using PECAM-1 (CD31) and crosses the basement membrane with proteases.
- Chemotaxis: it crawls up gradients of bacterial formyl peptides, C5a, leukotriene B4 and IL-8.
- Activation at the site: phagocytosis, killing by reactive oxygen species and enzymes, and release of more mediators.
Defects of recruitment and killing
| Condition | Defect | Clue |
|---|---|---|
| Leukocyte adhesion deficiency type 1 | β2 integrin subunit (CD18, gene ITGB2): no firm adhesion | Delayed separation of the umbilical cord, infections without pus, very high blood neutrophil count |
| Leukocyte adhesion deficiency type 2 | No sialyl-Lewis X (fucosylation defect): no rolling | Infections as in type 1, plus Bombay blood group, short stature and intellectual disability |
| Chédiak-Higashi syndrome | LYST gene: faulty lysosome trafficking, giant granules | Partial albinism, recurrent pyogenic infections, neuropathy, bleeding |
| Chronic granulomatous disease | NADPH oxidase: no respiratory burst | Infections by catalase-positive organisms, granulomas, abnormal DHR test |
| Glucocorticoids, adrenaline | Reduced adhesion: marginated neutrophils return to the blood (demargination) | Neutrophilia without infection |
Test yourself
Think of the answer, then tap the question to see it.
Which molecules mediate the rolling of leukocytes?
Selectins: E- and P-selectin on the endothelium and L-selectin on the leukocyte, binding sialylated sugars such as sialyl-Lewis X.
An infant has delayed umbilical cord separation, skin infections without pus and marked neutrophilia. What is the defect?
Leukocyte adhesion deficiency type 1: absent β2 integrin (CD18), so neutrophils cannot adhere firmly and leave the vessels.
Why do glucocorticoids raise the blood neutrophil count?
They reduce adhesion molecules, so neutrophils that were stuck to vessel walls (the marginated pool) return to the circulation.
Which molecules act as chemoattractants for neutrophils?
Bacterial N-formylmethionine peptides, complement C5a, leukotriene B4 and IL-8 (CXCL8).
Related
- Vascular changes in acute inflammation: vasodilation, leakage, exudate vs transudate
- Mediators of inflammation: the table to know
- When leukocytes injure tissue: proteases, oxidants and NETs
- Inflammation: the cardinal signs and its five steps
- Chronic inflammation: causes, cells and features
Related conditions
- Leukocyte adhesion deficiency
- Chédiak–Higashi syndrome
- Chronic granulomatous disease
- Hyper-IgE syndrome (Job syndrome)
- Abscess, furuncle and carbuncle
- Acute appendicitis
- Community-acquired pneumonia
Elsewhere in DurgiPedia
- Neutrophil
- Phagocyte defects: CGD, LAD, Chédiak–Higashi
- IL-8 and the chemokines
- Phagocytosis and the respiratory burst
- Lymphocyte recirculation and homing
- Complement: three pathways, MAC, regulators
In Pharmacology
Educational content on the mechanisms of disease; not a diagnostic or treatment guide and no substitute for a health professional's advice. No doses are given.
Sources: Leukocyte adhesion deficiency type 1: MedlinePlus Genetics (MedlinePlus, US National Library of Medicine, 2026); Chronic granulomatous disease: MedlinePlus Genetics (MedlinePlus, US National Library of Medicine, 2026); 17.5 Inflammation and Fever (OpenStax (Microbiology), 2016).
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Representative model, for educational purposes only.