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      C. butyricum lipoteichoic acid inhibits the inflammatory response and apoptosis in HT-29 cells induced by S. aureus lipoteichoic acid.

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          Abstract

          Lipoteichoic acid (LTA) is one of microbe-associated molecular pattern (MAMP) molecules of gram-positive bacteria. In this study, we demonstrated that Clostridium butyricum LTA (bLTA) significantly inhibited the inflammatory response and apoptosis induced by Staphylococcus aureus LTA (aLTA) in HT-29 cells. aLTA stimulated the inflammatory responses by activating a strong signal transduction cascade through NF-κB and ERK, but bLTA did not activate the signaling pathway. bLTA pretreatment inhibited the activation of the NF-κB and ERK signaling pathway induced by aLTA. The expression and release of cytokines such as IL-8 and TNF-α were also suppressed by bLTA pretreatment. aLTA treatment induced apoptosis in HT-29 cells, but bLTA did not affect the viability of the cells. Further study indicated that bLTA inhibited apoptosis in HT-29 cells induced by aLTA. These results suggest that bLTA may act as an aLTA antagonist and that an antagonistic bLTA may be a useful agent for suppressing the pro-inflammatory activities of gram-positive pathogenic bacteria.

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          Author and article information

          Journal
          Int. J. Biol. Macromol.
          International journal of biological macromolecules
          Elsevier BV
          1879-0003
          0141-8130
          Jul 2016
          : 88
          Affiliations
          [1 ] Ningbo Institute of Technology, Zhejiang University, Ningbo, Zhejiang 315100, China. Electronic address: wangjb777@126.com.
          [2 ] Ningbo Institute of Technology, Zhejiang University, Ningbo, Zhejiang 315100, China.
          [3 ] Centre for Biomolecular Sciences, University of Nottingham, NG7 2RD, United Kingdom.
          Article
          S0141-8130(16)30278-1
          10.1016/j.ijbiomac.2016.03.054
          27020942
          40758c74-7072-4cbc-aedf-8c46b7fd8a15
          History

          Lipoteichoic acid,Inflammatory response,HT-29 cells,Clostridium butyricum,Apoptosis,Staphylococcus aureus

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