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Am. J. Respir. Crit. Care Med., Volume 156, Number 1, July 1997, 234-239

Role of Cytokine-induced Neutrophil Chemoattractant (CINC) in Ozone-induced Airway Inflammation and Hyperresponsiveness

HIROSHI KOTO, MICHAEL SALMON, EL-BADOUI HADDAD, TUNG-JUNG HUANG, JOHN ZAGORSKI, and K. FAN  CHUNG

Department of Thoracic Medicine, National Heart and Lung Institute, Imperial College of Science, Technology and Medicine, London, England, and National Institutes of Health, Bethesda, Maryland

Cytokine-induced neutrophil chemoattractant (CINC) is a rat chemokine with potent chemoattractant effects on neutrophils. We determined the involvement of CINC in ozone-induced airway neutrophilia and bronchial hyperresponsiveness (BHR) in the rat. We found a marked increase in lung CINC messenger RNA (mRNA) within 2 h after cessation of ozone exposure (1 ppm for 3 h), as measured by Northern blot analysis, whereas rats exposed to room air had no detectable CINC mRNA. Ozone exposure induced a significant neutrophilia in bronchoalveolar lavage fluid (BALF) at 24 h after exposure (air-exposed rats: 4.2 ± 2.0 × 104, versus ozone-exposed rats: 16.1 ± 3.7 × 104); prior treatment with a goat anti-CINC antibody (1 mg, intravenously) suppressed the neutrophilia (3.1 ± 0.9 × 104). When administered intratracheally, the antibody (230 µg) partially inhibited the influx of neutrophils. The increase in bronchial responsiveness to acetylcholine observed after ozone exposure was not inhibited by the anti-CINC antibody. The anti-CINC antibody (1 mg, intravenously) also inhibited BALF neutrophilia induced by exposure to a higher concentration of ozone (3 ppm, 3 h), without an effect on BHR. CINC is an important chemokine causing ozone-induced neutrophil chemoattraction, but is not involved in the induction of ozone-induced BHR. The neutrophil is unlikely to contribute to BHR in this model.




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Copyright © 1997 American Thoracic Society