Pneumocystis carinii beta-glucan induces release of macrophage inflammatory protein-2 from primary rat alveolar epithelial cells via a receptor distinct from CD11b/CD18
Pneumocystis carinii (PC) pneumonia remains a life threatening infection in immunocompromised hosts. Neutrophilic inflammation and diffuse alveolar damage contribute significantly to respiratory failure characteristic of severe PC pneumonia. We have recently shown that alveolar macrophages produce t...
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Veröffentlicht in: | The Journal of eukaryotic microbiology 2001-01, Vol.Suppl, p.157S-157S |
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Format: | Artikel |
Sprache: | eng |
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Zusammenfassung: | Pneumocystis carinii (PC) pneumonia remains a life threatening infection in immunocompromised hosts. Neutrophilic inflammation and diffuse alveolar damage contribute significantly to respiratory failure characteristic of severe PC pneumonia. We have recently shown that alveolar macrophages produce tumor necrosis factor (TNF) and macrophage inflammatory protein-2 (MIP-2) in response to purified particulate PC beta -glucan. Although several different receptors have been reported to bind beta -glucan, the best studied among is the CD11b/CD18 complex (CR3). The membrane glycosphingolipid, lactosylceramide (CDw17), has also been shown to participate in the glucan receptor complex. Recent studies have demonstrated that alveolar epithelial cells (AEC's) play an important role in lung inflammation by the release of cytokines and chemokines. The purpose of this study is to determine if purified particulate PC beta -glucan induces MIP-2 expression from primary AEC's. |
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ISSN: | 1066-5234 |