Abstract
Corticotropin-releasing hormone (Crh), a major mediator of the stress response, has been shown to exert both stimulatory and inhibitory effects on the regulation of the immune system, in vivo. In our present study, we used the Crh-/- mice to investigate the effect of Crh deficiency on leukocyte function in vitro. Our results show that following LPS treatment, TNF-alpha and IL-1beta expression was significantly compromised in Crh-/- splenocytes, an effect most likely mediated by the lower levels of NF-kappaB DNA binding activity measured in the same cells. Furthermore, we show here that the proliferation rate of Crh-/- splenocytes in response to LPS was decreased compared to Crh+/+ splenocytes. Taken together, our findings show that the presence of endogenous Crh is necessary for the normal function of leukocytes, in vitro.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Cell Division / genetics
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Cell Division / immunology
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Cells, Cultured
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Corticotropin-Releasing Hormone / biosynthesis
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Corticotropin-Releasing Hormone / deficiency*
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Corticotropin-Releasing Hormone / pharmacology
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Corticotropin-Releasing Hormone / physiology*
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Cytokines / biosynthesis
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Cytokines / genetics
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Cytokines / metabolism
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Down-Regulation / genetics
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Down-Regulation / immunology
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Interleukin-1 / metabolism
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Lipopolysaccharides / pharmacology*
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Lymphocyte Activation / genetics
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Lymphocyte Subsets / immunology
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Lymphocyte Subsets / metabolism
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Lymphocyte Subsets / pathology
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Mice
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Mice, Inbred C57BL
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Mice, Knockout
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NF-kappa B / antagonists & inhibitors
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NF-kappa B / metabolism
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RNA, Messenger / antagonists & inhibitors
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RNA, Messenger / biosynthesis
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Spleen / drug effects
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Spleen / immunology*
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Spleen / metabolism*
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Spleen / pathology
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Tumor Necrosis Factor-alpha / metabolism
Substances
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Cytokines
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Interleukin-1
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Lipopolysaccharides
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NF-kappa B
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RNA, Messenger
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Tumor Necrosis Factor-alpha
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Corticotropin-Releasing Hormone