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In this study, to elucidate further the functional significance and pathophysiological implications of these findings, we demonstrated that microglial cells are not only the source but also the target cells of activin A in the central nervous system: immunohistochemistry and RT\u2010PCR revealed expression of activin subunit \u03b2A mRNA as well as activin receptor type I and type II mRNA in rat microglia in vitro. Further studies showed that activin enhances microglial proliferation and decreases the \u03b3\u2010interferon\u2010induced synthesis of nitric oxide, one of several microglial mediators involved in the inflammatory response in microglia activation. Furthermore, quantitative RT\u2010PCR, Western blotting, and ELISA showed an inhibitory effect of activin on inducible nitric oxide synthase, tumor necrosis factor\u2010\u03b1, interleukin\u20106, and interleukin\u20101\u03b2 gene and protein levels after lipopolysaccharide treatment. We suggest that the increased synthesis of activin A is directly involved, via influence on microglia cell functions, in the modulation of the inflammatory response in bacterial meningitis. \u00a9 2009 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jnr.22185","type":"journal-article","created":{"date-parts":[[2009,8,13]],"date-time":"2009-08-13T21:25:31Z","timestamp":1250198731000},"page":"16-23","source":"Crossref","is-referenced-by-count":25,"title":["Regulation of activin A synthesis in microglial cells: Pathophysiological implications for bacterial 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