Publication: Regulation of CRIg expression and phagocytosis in human macrophages by arachidonate, dexamethasone, and cytokines
Issued Date
2011-09-01
Resource Type
ISSN
15252191
00029440
00029440
Other identifier(s)
2-s2.0-80052868421
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Mahidol University
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SCOPUS
Bibliographic Citation
American Journal of Pathology. Vol.179, No.3 (2011), 1310-1318
Suggested Citation
Nick N. Gorgani, Umaporn Thathaisong, Violet R.S. Mukaro, Ornnuthchar Poungpair, Amanda Tirimacco, Charles S.T. Hii, Antonio Ferrante Regulation of CRIg expression and phagocytosis in human macrophages by arachidonate, dexamethasone, and cytokines. American Journal of Pathology. Vol.179, No.3 (2011), 1310-1318. doi:10.1016/j.ajpath.2011.05.021 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/12366
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Title
Regulation of CRIg expression and phagocytosis in human macrophages by arachidonate, dexamethasone, and cytokines
Abstract
Although the importance of the macrophage complement receptor immunoglobulin (CRIg) in the phagocytosis of complement opsonized bacteria and in inflammation has been established, the regulation of CRIg expression remains undefined. Because cellular activation during inflammation leads to the release of arachidonate, a stimulator of leukocyte function, we sought to determine whether arachidonate regulates CRIg expression. Adding arachidonate to maturing human macrophages and to prematured CRIg + macrophages caused a significant decrease in the expression of cell-surface CRIg and CRIg mRNA. This effect was independent of the metabolism of arachidonate via the cyclooxygenase and lipoxygenase pathways, because it was not inhibited by the nonsteroidal anti-inflammatory drugs indomethacin and nordihydroguaiaretic acid. Studies with specific pharmacological inhibitors of arachidonate-mediated signaling pathways showed that protein kinase C was involved. Administration of dexamethasone to macrophages caused an increase in CRIg expression. Studies with proinflammatory and immunosuppressive cytokines showed that IL-10 increased, but interferon-γ, IL-4, and transforming growth factor-β1 decreased CRIg expression on macrophages. This down- and up-regulation of CRIg expression was reflected in a decrease and increase, respectively, in the phagocytosis of complement opsonized Candida albicans. These data suggest that a unique inflammatory mediator network regulates CRIg expression and point to a mechanism by which arachidonate and dexamethasone have reciprocal effects on inflammation. © 2011 American Society for Investigative Pathology.