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- W1492134927 abstract "Abstract Low grade endotoxemia, mainly caused by subclinical level of blood circulating LPS, is prevalent in the individuals with adverse health conditions or lifestyles. Here, we found that low doses LPS (50 pg/ml~1 ng/ml) preferentially expanded Ly6C+ monocyte population in bone marrow cultures supplemented with M-CSF. TGF-β production in monocytes was diminished by low dosed LPS. Interestingly, high doses LPS (10 ng/ml~1 µg/ml) decreased Ly6C+ monocyte population. Low doses LPS dramatically enhanced IL-12 production but reduced iNOS expression in macrophages, while high doses LPS exerted an opposite impact. In a mouse model with wound punctures on the back skin, super low grade LPS administration (5 µg/kg) remarkably delayed wound repair, as shown by three days’ lag in wound closure compared to PBS injected mice. We observed a two-fold reduction of collagen deposition around wound sites, suggesting disruption of tissue remodeling. Consistent with in vitro studies, we detected increased numbers of Ly6C+ monocytes circulating in peripheral blood and accumulated in wound lesions in the mice with LPS treatment. Moreover, TGF-β production in the skin, which facilitates wound repairing, was also remarkably impaired by low grade LPS administration. These data demonstrated that subclinical level of LPS was sufficient to prime monocytes/macrophages and compromise wound healing process, potentially due to the expansion of monocytes/macrophages with low-grade pro-inflammatory properties." @default.
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- W1492134927 date "2014-05-01" @default.
- W1492134927 modified "2023-09-27" @default.
- W1492134927 title "Low grade endotoxemia delays wound healing associated with inflammatory monocytes/macrophages expansion (INC7P.405)" @default.
- W1492134927 doi "https://doi.org/10.4049/jimmunol.192.supp.186.6" @default.
- W1492134927 hasPublicationYear "2014" @default.
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