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Learn MoreThe skin is the human bodys largest organ and is in contact with a diverse community of microorganisms that includes both resident and pathogenic bacteria. Skin immune defenses include the production of antimicrobial proteins that kill bacteria directly. However, we still have an incomplete understanding of how skin antimicrobial proteins promote homeostasis with resident bacterial communities and limit infection. Here, we show that resistin-like molecule (RELM) is an antibacterial protein that is produced by keratinocytes and sebocytes in the mouse skin. RELM expression was induced in mouse skin by resident and pathogenic skin bacteria and was bactericidal for several bacterial species found on the skin, including Streptococcus pyogenes. Mice lacking RELM had altered resident skin bacterial communities and were more susceptible to bacterial infection, indicating that RELM controls bacterial colonization of the skin. RELM expression required dietary vitamin A and could be induced by therapeutic retinoids that protected against bacterial infection in a RELM-dependent manner. Resistin, another member of the RELM family, was expressed in human skin, required retinoids for expression, and killed skin bacteria, indicating a conserved function for RELM proteins in skin innate immunity. Our findings thus identify members of the RELM family as antibacterial proteins that provide vitamin A-dependent antimicrobial protection of the skin, and provide insight into why skin immunity requires adequate dietary vitamin A. SOURCE: Zheng KuangLora Hooper UT Southwestern medical center
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