| Literature DB >> 12065904 |
Etsuro Sato1, Masayuki Haniuda, Hiroki Numanami, Toshiki Ushiyama, Akihiro Tsukadaira, Shuji Takashi, Yoshio Okubo, Sekiya Koyama.
Abstract
Histamine and serotonin are important inflammatory mediators in the pathophysiology of asthma, and asthmatic patients have higher plasma histamine and serotonin levels than nonasthmatic control subjects. Eotaxin, a potent eosinophil-specific chemotactic factor, is increased in the lower respiratory tract of allergic patients. Recently, lung fibroblasts have been reported to produce eotaxin and are suggested to be the major cellular source of eotaxin. We postulated that lung fibroblasts might release eotaxin in response to histamine or serotonin. To test this hypothesis, we evaluated the potential of histamine or serotonin to induce the release of eotaxin by the human fetal lung fibroblast cell line, HFL-1. HFL-1 released eotaxin in response to histamine and serotonin in a dose- and time-dependent manner (p < 0.05). Histamine or serotonin treatment of HFL-1 augmented the expression of eotaxin mRNA. Eosinophil chemotactic activity by HFL-1 supernatant fluids was inhibited by anti-human eotaxin-neutralizing antibody. These findings lead to the hypothesis that lung-fibroblast-derived eotaxin may in part be responsible for the eosinophil infiltration observed in allergic disease of the airways. Copyright 2002 S. Karger AG, BaselEntities:
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Year: 2002 PMID: 12065904 DOI: 10.1159/000059413
Source DB: PubMed Journal: Int Arch Allergy Immunol ISSN: 1018-2438 Impact factor: 2.749