AI Article Synopsis
- Complement 1 inhibitor (C1INH) regulates complement cascades and protease activation, with the highest expression of EcC1INH mRNA found in the liver.
- Exposure to Vibrio alginolyticus significantly boosts EcC1INH mRNA levels in both liver and kidney tissues.
- The N-terminal domain of EcC1INH reduces LPS binding to cells and can inhibit LPS-induced inflammation by interfering with proinflammatory cytokine production.
Article Abstract
Complement 1 inhibitor (C1INH) serving as a multifunctional factor can participate in the regulation of complement cascades and attenuate the activation of various proteases. In this study, we obtained EcC1INH cDNA and the tissue-specific analysis indicate that the highest expression level of EcC1INH mRNA was detected in liver. Moreover, Vibrio alginolyticus challenge can significantly increase EcC1INH mRNA expression in liver and kidney. N-terminal domain of EcC1INH could decrease LPS binding activity to cell surface, while loss of positively charged residues (PCRs) Arg21, His22, Lys50, Arg61 in N-terminal domain of EcC1INH can significantly reduce its interaction with LPS. Furthermore, LPS injection experiment indicated that the binding of EcC1INH N-terminal domain to LPS can antagonize LPS-induced inflammatory signaling pathway and attenuate the production of proinflammatory cytokines in vivo, indicating that EcC1INH was involved in negative regulation of inflammatory response.
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| http://dx.doi.org/10.1016/j.fsi.2018.09.063 | DOI Listing |
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