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
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.