NDLI: M-CSF inhibits anti-HIV-1 activity of IL-32, but they enhance M2-like phenotypes of macrophages.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Nasser, Hesham Maekawa, Takaaki Bhuyan, Farzana Osman, Abu Suzu, Shinya Hashimoto, Michihiro
Description	Country affiliation: Japan Author Affiliation: Osman A ( Center for AIDS Research, Kumamoto University, Kumamoto 860-0811, Japan.); Bhuyan F ( Center for AIDS Research, Kumamoto University, Kumamoto 860-0811, Japan.); Hashimoto M ( Center for AIDS Research, Kumamoto University, Kumamoto 860-0811, Japan.); Nasser H ( Center for AIDS Research, Kumamoto University, Kumamoto 860-0811, Japan.); Maekawa T ( Center for AIDS Research, Kumamoto University, Kumamoto 860-0811, Japan.); Suzu S ( Center for AIDS Research, Kumamoto University, Kumamoto 860-0811, Japan ssuzu06@kumamoto-u.ac.jp.)
Abstract	M-CSF promotes the differentiation and survival of macrophages, and preferentially induces anti-inflammatory M2, rather than proinflammatory M1 macrophages. Recently, another cytokine, IL-32, was also shown to promote macrophage differentiation. In this article, we provide the first evidence, to our knowledge, that M-CSF has both additive and inhibitory effects on the macrophage-related activities of IL-32. When added to M-CSF-derived macrophages, M-CSF and IL-32 promoted macrophage survival, which was further enhanced by their combination. However, they had different effects on HIV-1 replication; that is, it was stimulated by M-CSF and inhibited by IL-32. Interestingly, the anti-HIV-1 activity of IL-32 was counteracted by M-CSF. Such inhibitory effect of M-CSF was not observed with IL-32-induced M1-like features including high cytokine/chemokine production and strong expression of the costimulatory molecule CD80. However, IL-32-treated macrophages unexpectedly showed also M2-like features including increased phagocytic activity, and high expression of CD14 and the scavenger receptor CD163, and the expression of CD14 and CD163 was further upregulated by cotreatment with M-CSF. The findings of this study regarding the unique functional interplay between M-CSF and IL-32 increase our understanding of the mechanisms that regulate the survival and M1/M2 ratio of macrophages, as well as HIV-1 replication in macrophages.
ISSN	00221767
e-ISSN	15506606
Journal	The Journal of Immunology
Issue Number	11
Volume Number	192
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2014-06-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Hiv Infections Immunology Hiv-1 Physiology Interleukins Macrophage Colony-stimulating Factor Macrophages Virus Replication Animals Antigens, Cd Cell Survival Drug Effects Cells, Cultured Gene Expression Regulation Pharmacology Pathology Virology Phagocytosis Clinical Trial Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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