IL-8 is one of the major chemokines produced by monkey airway epithelium after ozone-induced injury

被引:31
作者
Chang, MMJ [1 ]
Wu, R
Plopper, CG
Hyde, DM
机构
[1] Univ Calif Davis, Sch Med, Ctr Comparat Resp Biol & Med, Davis, CA 95616 USA
[2] Univ Calif Davis, Sch Vet Med, Dept Anat Physiol & Cell Biol, Davis, CA 95616 USA
关键词
chemotaxis; neutrophil; differential hybridization; in situ hybridization; immunohistochemistry; interleukin-8;
D O I
10.1152/ajplung.1998.275.3.L524
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
A rhesus monkey interleukin (IL)-8 cDNA clone with >94% homology to the human IL-8 gene was isolated by differential hybridization from a cDNA library of distal airways after ozone inhalation. In situ hybridization and immunohistochemistry showed increased IL-8 mRNA and protein levels in epithelial cells at 1 h but not at 24 h after inhalation of ozone. The appearance of IL-8 in airway epithelial cells correlated well with neutrophil influx into airway epithelia and lumens. Air-liquid interface cultures of tracheobronchial epithelial cells were exposed to ozone in vitro. We observed a transient increase in IL-8 secretion in culture medium immediately after ozone exposure and a dose-dependent increase in IL-8 secretion and mRNA production. In vitro neutrophil chemotaxis showed a parallel dose and time profile to epithelial cell secretion of IL-8. Treatment with anti-IL-8 neutralizing antibody blocked >80% of the neutrophil chemotaxis in vitro. These results suggest that IL-8 is a key chemokine in acute ozone-induced airway inflammation in primates.
引用
收藏
页码:L524 / L532
页数:9
相关论文
共 32 条
[1]   THE EFFECT OF CONDITIONED MEDIUM FROM CULTURED HUMAN BRONCHIAL EPITHELIAL-CELLS ON EOSINOPHIL AND NEUTROPHIL CHEMOTAXIS AND ADHERENCE IN-VITRO [J].
ABDELAZIZ, MM ;
DEVALIA, JL ;
KHAIR, OA ;
CALDERON, M ;
SAPSFORD, RJ ;
DAVIES, RJ .
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 1995, 13 (06) :728-737
[2]  
ANGERER LM, 1987, METHOD ENZYMOL, V152, P649
[3]   OZONE-INDUCED AIRWAY INFLAMMATION IN HUMAN-SUBJECTS AS DETERMINED BY AIRWAY LAVAGE AND BIOPSY [J].
ARIS, RM ;
CHRISTIAN, D ;
HEARNE, PQ ;
KERR, K ;
FINKBEINER, WE ;
BALMES, JR .
AMERICAN REVIEW OF RESPIRATORY DISEASE, 1993, 148 (05) :1363-1372
[4]   ALTERATION OF OZONE-INDUCED AIRWAY PERMEABILITY BY OXYGEN METABOLITES AND ANTIOXIDANTS [J].
BHALLA, DK .
TOXICOLOGY LETTERS, 1994, 73 (02) :91-101
[5]   COMPARISON OF LEUKOTRIENE B4-INDUCED NEUTROPHIL MIGRATION THROUGH DIFFERENT CELLULAR BARRIERS [J].
CASALE, TB ;
ABBAS, MK .
AMERICAN JOURNAL OF PHYSIOLOGY, 1990, 258 (04) :C639-C647
[6]   Formation of intracellular free radicals in guinea pig airway epithelium during in vitro exposure to ozone [J].
Chen, LC ;
Qu, QS .
TOXICOLOGY AND APPLIED PHARMACOLOGY, 1997, 143 (01) :96-101
[7]   RESPIRATORY EFFECTS OF AIR-POLLUTION - EFFECT OF OXIDANT AIR-POLLUTANTS ON THE RESPIRATORY SYSTEM - INSIGHTS FROM EXPERIMENTAL ANIMAL RESEARCH [J].
CHITANO, P ;
HOSSELET, JJ ;
MAPP, CE ;
FABBRI, LM .
EUROPEAN RESPIRATORY JOURNAL, 1995, 8 (08) :1357-1371
[8]  
CHOMCZYNSKI P, 1987, ANAL BIOCHEM, V162, P156, DOI 10.1016/0003-2697(87)90021-2
[9]   AIRWAY EPITHELIAL-CELLS AND MEDIATORS OF INFLAMMATION [J].
DEVALIA, JL ;
DAVIES, RJ .
RESPIRATORY MEDICINE, 1993, 87 (06) :405-408
[10]   Mechanisms of pollution-induced airway disease: In vitro studies in the upper and lower airways [J].
Devalia, JL ;
Bayram, H ;
Rusznak, C ;
Calderon, M ;
Sapsford, RJ ;
Abdelaziz, MA ;
Wang, J ;
Davies, RJ .
ALLERGY, 1997, 52 :45-51