CCR2 recruits an inflammatory macrophage subpopulation critical for angiogenesis in tissue repair. Staphylococcus aureus degrades neutrophil extracellular traps to promote immune cell death. Macrophage-derived LTB4 promotes abscess formation and clearance of Staphylococcus aureus skin infection in mice. MyD88 in macrophages is critical for abscess resolution in staphylococcal skin infection. Neutrophil-derived IL-1β is sufficient for abscess formation in immunity against Staphylococcus aureus in mice. Critical roles for CCR2 and MCP-3 in monocyte mobilization from bone marrow and recruitment to inflammatory sites. Ghrelin inhibits leptin- and activation-induced proinflammatory cytokine expression by human monocytes and T cells. Developmental and functional heterogeneity of monocytes. Monocyte recruitment during infection and inflammation. In sum, we find that monocytes function as a cellular rheostat by regulating leptin levels and revascularization during wound repair. Ghrelin, which opposes leptin function 3, was produced locally by monocytes, and reduced vascular overgrowth and improved healing post-infection. In infected monocyte-deficient mice there was increased persistent hypodermis thickening and an elevated leptin level, which drove overgrowth of dysfunctional blood vasculature and delayed healing, with a thickened scar. Monocytes did not contribute to bacterial clearance but converted to macrophages that persisted for weeks after infection, regulating hypodermal adipocyte expansion and production of the adipokine hormone leptin. Here, using a foreign body coated with Staphylococcus aureus and imaging over time from cutaneous infection to wound resolution, we show that monocytes and neutrophils are recruited in similar numbers with low-dose infection but not with high-dose infection, and form a localization pattern in which monocytes surround the infection site, whereas neutrophils infiltrate it. However, unlike neutrophils, monocytes have the capacity to convert to situationally specific macrophages that may have critical functions beyond infection control 1, 2. During infection, inflammatory monocytes are thought to be key for bacterial eradication, but this is hard to reconcile with the large numbers of neutrophils that are recruited for each monocyte that migrates to the afflicted tissue, and the much more robust microbicidal functions of the neutrophils.
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