Short exposure of intestinal epithelial cells to TNF-alpha and histamine induces Mac-1-mediated neutrophil adhesion independent of protein synthesis

Citation
R. Miyata et al., Short exposure of intestinal epithelial cells to TNF-alpha and histamine induces Mac-1-mediated neutrophil adhesion independent of protein synthesis, J LEUK BIOL, 66(3), 1999, pp. 437-446
Citations number
49
Categorie Soggetti
Immunology
Journal title
JOURNAL OF LEUKOCYTE BIOLOGY
ISSN journal
07415400 → ACNP
Volume
66
Issue
3
Year of publication
1999
Pages
437 - 446
Database
ISI
SICI code
0741-5400(199909)66:3<437:SEOIEC>2.0.ZU;2-F
Abstract
Neutrophils play an important role in intestinal inflammation by interactin g with intestinal epithelial cells. In this study, we evaluated neutrophil adhesion to intestinal epithelial cells using intestinal epithelial cell li ne HT29 stimulated with tumor necrosis factor alpha (TNF-alpha) and histami ne for a short time (30 min), The TNF-at and histamine stimulation markedly increased neutrophil adhesion. The increased adhesion was inhibited by ant i-CD11b and anti-CD18 monoclonal antibodies (mAbs), but not by anti-CD11a a nd anti-CD54 (ICAM-1) mAbs, It is interesting that flow cytometric analysis revealed that ICAM-1 expression on HT29 cells was not changed by TNF-alpha and histamine stimulation, Moreover, the increased adhesion was inhibited by proteinase K treatment but not cycloheximide treatment of HT29 cells, To gether these observations suggest that short exposure of HT29 cells to TNF- alpha and histamine induces CD11b/CD18 (Mac-1)-dependent but CD11a/CD18 (LF A-1)-independent neutrophil adhesion to intestinal epithelial cells, and IC AM-1 is not likely to be involved in the interactions. Furthermore, epithel ial cell ligand(s) for neutrophils is likely protein molecule(s) that is ex pressed on the cell by stimulation independent protein synthesis. However, it is also possible that neutrophil activating factor(s), which stimulates neutrophils to bind with epithelial ligands via Mac-1, is expressed by epit helial cells during stimulation.