[Stimulation of ozone stress on the adhesion of inflammatory cells to bronchial epithelial cells].
OBJECTIVE
To determine into the inflammation process of bronchial epithelial cells (BECs) and observe the modulatory effect of some protective factors on BECs.


METHODS
We built the cell injury model with ozone and observed the effect of ozone stress on polymorphonuclear loeukocyte (PMNs) and eosinophil (EOS) adhesion to BECs. The effect of intercellular adhesion molecule (ICAM-1) antibody on the adhesion and ICAM-1 protein expression of BECs was observed at the same time.


RESULTS
O3 increased the adhesion of BECs to PMNs and EOS. Adhesion could be blocked by ICAM-1 antibody, suggesting ICAM-1 was the principal molecule leading PMNs and EOS adhesion to BECs. The immunocytochemistry assay indicated that O3 increased the expression of ICAM-1 protein of BECs.


CONCLUSIONS
Ozone stress leads to inflammation, and the principal adhesion molecule is ICAM-1 resulting in adhesion between BECs and PMNs, and between BECs and EOS.
Zhang
Chang-qing
CQ
Department of Physiology, Xiangya School of Medicine, Central South University, Changsha 410078, China.
Tan
Yu-rong
YR
Qin
Xiao-qun
XQ
D000818:Animals; D001980:Bronchi / Q000166:cytology* / Q000378:metabolism; D002448:Cell Adhesion / Q000502:physiology; D002478:Cells, Cultured; D004804:Eosinophils / Q000166:cytology; D004847:Epithelial Cells / Q000166:cytology*; D005260:Female; D007249:Inflammation / Q000473:pathology*; D018799:Intercellular Adhesion Molecule-1 / Q000032:analysis; D008297:Male; D009504:Neutrophils / Q000166:cytology; D010126:Ozone; D011817:Rabbits; D013312:Stress, Physiological
D018799:Intercellular Adhesion Molecule-1; D010126:Ozone