Mechanisms underlying neutrophil adhesion to apical epithelial membranes

Crypt abscesses allow prolonged apposition of activated neutrophils to the epithelial surface of the colon. Adhesion of neutrophils to both the vascular endothelium and basolateral epithelial membrane share common effector molecules but are distinct processes. This study aimed to define the mechanis...

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Veröffentlicht in:Gut Jg. 38; H. 2; S. 201 - 205
Hauptverfasser: Meenan, J, Mevissen, M, Monajemi, H, Radema, S A, Soule, H R, Moyle, M, Tytgat, G N, van Deventer, S J
Format: Journal Article
Sprache:Englisch
Veröffentlicht: London BMJ Publishing Group Ltd and British Society of Gastroenterology 01.02.1996
BMJ
BMJ Publishing Group LTD
Schlagworte:
Biological and medical sciences
Cell Adhesion - drug effects
Cell Adhesion Molecules - pharmacology
Clone Cells
Colonic Neoplasms - immunology
Gastroenterology. Liver. Pancreas. Abdomen
Glycoproteins - pharmacology
Helminth Proteins - pharmacology
Humans
Intercellular Adhesion Molecule-1 - pharmacology
Lymphocyte Function-Associated Antigen-1 - pharmacology
Medical sciences
Membrane Proteins
Neutrophil Activation
Neutrophils - drug effects
Neutrophils - physiology
Other diseases. Semiology
Stomach. Duodenum. Small intestine. Colon. Rectum. Anus
Tumor Cells, Cultured
Human
Digestive system
Gut
Inflammation
Adhesion
In vitro
Integrin
Blood vessel
Epithelial cell
Circulatory system
Colon
Neutrophil
Mechanism of action
ISSN:0017-5749, 1468-3288, 1458-3288
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Zusammenfassung:Crypt abscesses allow prolonged apposition of activated neutrophils to the epithelial surface of the colon. Adhesion of neutrophils to both the vascular endothelium and basolateral epithelial membrane share common effector molecules but are distinct processes. This study aimed to define the mechanisms that effect adhesion, independent of transmigration, to the apical epithelium. HT29 (cl 19A) cells were grown to confluency and incubated with neutrophils under conditions of: (i) neutrophil stimulation with phorbol-myristate-acetate; (ii) monolayer stimulation with interferon gamma, tumour necrosis factor alpha (IFN gamma, TNF alpha); and (iii) recent epithelial cell trypsinisation. These experiments were carried out in the presence of neutralising antibodies to CD18, CD11b, LFA-1, E-selectin, P-selectin, intracellular adhesion molecule 1 (ICAM-1), and ICAM-2; a novel CD11b/CD18 antagonist, neutrophil inhibitory factor (rNIF); adenosine receptor agonists (5'N-ethycarboxamido adenosine/N6-cylopentyladenosine (NECA/CPA)) and a platelet activating factor (PAF) receptor antagonist lexipafant. Adhesion of stimulated neutrophils to resting monolayers was Mac-1, CD18 dependent and ICAM-1, ICAM-2, E-selectin, P-selectin, PAF independent. Cytokine activated monolayers exhibited higher binding of neutrophils which was inhibited by rNIF and aCD18. Recently trypsinised monolayers bound neutrophils in a CD11b/CD18 and CD18 independent manner. Adenosine agonists failed to influence neutrophil adhesion under any condition. This study shows neutrophil adhesion to apical epithelial membranes is similar to that at the epithelial basolateral membrane, though different to that seen at the vascular endothelium. These results highlight regional differences in neutrophil adhesion molecule usage.
Bibliographie:local:gutjnl;38/2/201
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PMID:8801197
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ISSN:0017-5749
1468-3288
1458-3288
DOI:10.1136/gut.38.2.201