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. However, unlike neutrophils, monocytes have the capacity to convert to situationally specific macrophages that may have critical functions beyond infection control^1,2. 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. 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. 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. Ghrelin, which opposes leptin function³, was produced locally by monocytes, and reduced vascular overgrowth and improved healing post-infection. In sum, we find that monocytes function as a cellular rheostat by regulating leptin levels and revascularization during wound repair.

在感染期间，炎性单核细胞被认为是消灭细菌的关键，但这很难与迁移到受感染组织的每个单核细胞募集的大量中性粒细胞以及中性粒细胞更强大的杀菌功能相协调。然而，与中性粒细胞不同，单核细胞有能力转化为特定情况的巨噬细胞，这些巨噬细胞可能具有超出感染控制^1,2的关键功能。在这里，使用涂有金黄色葡萄球菌的异物从皮肤感染到伤口消退随着时间的推移和成像，我们发现单核细胞和中性粒细胞在低剂量感染时募集的数量相似，但在高剂量感染时没有，并形成单核细胞围绕感染部位的定位模式，而中性粒细胞渗透它。单核细胞对细菌清除没有贡献，而是转化为巨噬细胞，在感染后持续数周，调节皮下脂肪细胞的扩张和脂肪因子激素瘦素的产生。在受感染的单核细胞缺陷小鼠中，皮下组织持续增厚，瘦素水平升高，导致功能失调的血管过度生长，愈合延迟，疤痕增厚。Ghrelin，反对瘦素功能³，由单核细胞局部产生，减少血管过度生长并改善感染后的愈合。总之，我们发现单核细胞在伤口修复过程中通过调节瘦素水平和血运重建来发挥细胞变阻器的作用。