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Mechanisms of ozone‐induced inhibitory effect of bronchoalveolar lavage fluid on alveolar macrophage‐mediated immunosuppressive activity in rats
Author(s) -
Koike Eiko,
Kobayashi Takahiro,
Murakami Masataka,
McWilliam Andrew S.,
Holt Patrick G.
Publication year - 1999
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.66.1.75
Subject(s) - bronchoalveolar lavage , immunosuppression , alveolar macrophage , immunology , concanavalin a , cytokine , nitric oxide , macrophage , biology , lung , medicine , in vitro , endocrinology , biochemistry
Resident alveolar macrophages (AM) play an important immunomodulatory role via suppression of lymphocyte proliferation, and nitric oxide (NO) plays a crucial role in this immunosuppression of AM. Our previous report suggested that during ozone (O 3 )‐induced lung inflammation, bronchoalveolar lavage fluid (BALF) inhibited AM‐ mediated immunosuppression and concanavalin A (Con A)‐induced proliferation of lymph node cells (LNC) [E. Koike et al. (1998) Toxicol. Sci. 41, 217–223]. In these studies, we investigated the mechanisms of the inhibition of BALF from O 3 ‐exposed rats (O 3 ‐BALF). We investigated whether BALF might affect (1) the interferon‐γ (IFN‐γ) production by Con A‐stimulated LNC and IFN‐γ‐induced NO production by AM, and (2) the interleukin (IL)‐2 production by Con A‐stimulated LNC and IL‐2‐induced LNC proliferation. These results demonstrated that O 3 ‐BALF inhibited IFN‐γ production by Con A‐stimulated LNC, IFN‐γ‐induced NO production by AM, and IL‐2‐induced LNC proliferation. In addition, the major inhibitory factor against AM‐mediated immunosuppression in O 3 ‐BALF may be a protein of greater than 10 kDa. J. Leukoc. Biol. 66: 75–82; 1999.