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- W636006174 abstract "Objective The goal of the current study was to determine whether complement factor B (cfB) would interplay with Toll-like receptors (TLRs) during sepsis and whether or not such interplay would contribute to septic cardiomyopathy. Methods Cardiomyocytes (CMs) were isolated from wild-type (WT) mice or mice deficient of TLR2 or TLR4. Polymicrobial sepsis was created by cecum ligation and puncture (CLP). cfB mRNA and protein were determined by qRT-PCR and Western blot, respectively. Cytokines were determined using a fluorescent multiplex assay. Left ventricular function was assessed in a Langendorff perfusion system. Results Both Pam3cys and lipopolysaccharide (LPS) markedly increased cfB mRNA expression in CMs via TLR2- and TLR4-dependent manner (fold, 217±54 and 578±54, respectively), but not complement 3, 4 or 5. TLR2, TLR3, TLR4 ligands also induced marked cfB protein expression in and release from CMs. In vivo, CLP led to a marked and time-dependent increase in cfB mRNA and protein expression in septic heart via MyD88-dependent manner. Importantly, compared with septic WT mice, septic cfB-KO mice had improved LV function, better survival rate, and decreased cytokine production. Conclusion cfB is up-regulated in response to TLR activation and polymicrobial sepsis via TLR-dependent manner. cfB deficiency confers a beneficial effect in cardiac function during sepsis. This research has been supported by NIH R01-GM080906 and R01-GM097259." @default.
- W636006174 created "2016-06-24" @default.
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- W636006174 date "2013-04-01" @default.
- W636006174 modified "2023-10-16" @default.
- W636006174 title "Interplay between complement factor B and Toll‐like receptors and its role in septic cardiomyopathy" @default.
- W636006174 doi "https://doi.org/10.1096/fasebj.27.1_supplement.652.6" @default.
- W636006174 hasPublicationYear "2013" @default.
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