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Key inflammatory mediators implicated in its pathogenesis include interleukin (IL)17, IL-23, and tumor necrosis factor-alpha (TNF-), primarily released by activated dendritic cells and T-cells (Q

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In relation to the primary site of infection, Ab treatment modulated the inflammatory response into peritoneal cavity of septic mice, inducing almost complete bacterial burden elimination 24 h post CLP and a significant augment in NO levels, without alterations in IL-1 and TNF- levels in relation to CLP-saline treated mice

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