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• W2058201437 abstract "Previously, we have reported that the susceptibility of burned patients to infectious complications is increased when the production of CC-chemokine ligand 3 (CCL3) is impaired. In this study, the role of the sympathetic nervous system on impaired CCL3 production and antibacterial resistance following burn injuries was investigated. Normal mice were resistant (65% survival) to cecal ligation and puncture (CLP)-induced sepsis, while the same CLP killed 90% of thermally injured mice (TI-mice). However, TI-mice resisted CLP-induced sepsis (60% survival) when they were previously treated with CCL3 or sympathectomized with 6-hydroxydopamine (6-OHDA). Augmentation of host resistance against CLP-induced sepsis by 6-OHDA was abrogated by anti-CCL3 mAb treatment. Norepinephrine (NE) production was increased in circulation of TI-mice, and treatment of TI-mice with 6-OHDA resulted in the inhibition of NE secretion. CCL3 production was impaired in cultures of T cells from TI-mice or normal T cells treated with NE, even when stimulated with anti-CD3 mAb. However, CCL3 was produced by mAb-stimulated T cells from TI-mice previously treated with 6-OHDA. These results indicated that by inhibiting CCL3 production the sympathetic nervous system contributes to the increased susceptibility of TI-mice to sepsis." @default.
• W2058201437 created "2016-06-24" @default.
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• W2058201437 date "2005-03-07" @default.
• W2058201437 modified "2023-09-26" @default.
• W2058201437 title "Contribution of the sympathetic nervous system on the burn-associated impairment of CCL3 production" @default.
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• W2058201437 doi "https://doi.org/10.1016/j.cyto.2004.10.014" @default.
• W2058201437 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/15760677" @default.
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