title: C. butyricum lipoteichoic acid inhibits the inflammatory response and apoptosis in HT-29 cells induced by S. aureus lipoteichoic acid.
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.
authors.affiliation: Ningbo Institute of Technology, Zhejiang University, Ningbo, Zhejiang 315100, China. Electronic address: wangjb777@126.com.
authors.forename: Jinbo
authors.initials: J
authors.lastname: Wang
authors.affiliation: Ningbo Institute of Technology, Zhejiang University, Ningbo, Zhejiang 315100, China.
authors.forename: Lili
authors.initials: L
authors.lastname: Qi
authors.affiliation: Ningbo Institute of Technology, Zhejiang University, Ningbo, Zhejiang 315100, China.
authors.forename: Lehe
authors.initials: L
authors.lastname: Mei
authors.affiliation: Ningbo Institute of Technology, Zhejiang University, Ningbo, Zhejiang 315100, China.
authors.forename: Zhige
authors.initials: Z
authors.lastname: Wu
authors.affiliation: Centre for Biomolecular Sciences, University of Nottingham, NG7 2RD, United Kingdom.
authors.forename: Hengzheng
authors.initials: H
authors.lastname: Wang
mesh_terms: D017209:Apoptosis / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D046972:Clostridium butyricum / Q000737:chemistry* / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D005786:Gene Expression Regulation / Q000187:drug effects* / Q000276:immunology; D019073:HT29 Cells; D006801:Humans; D007249:Inflammation / Q000517:prevention & control; D016209:Interleukin-8 / Q000235:genetics / Q000276:immunology; D008070:Lipopolysaccharides / Q000302:isolation & purification / Q000494:pharmacology*; D019950:Mitogen-Activated Protein Kinase 1 / Q000235:genetics / Q000276:immunology; D048052:Mitogen-Activated Protein Kinase 3 / Q000235:genetics / Q000276:immunology; D016328:NF-kappa B / Q000235:genetics / Q000276:immunology; D015398:Signal Transduction; D013045:Species Specificity; D013211:Staphylococcus aureus / Q000737:chemistry* / Q000378:metabolism / Q000472:pathogenicity; D013682:Teichoic Acids / Q000302:isolation & purification / Q000494:pharmacology*; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000276:immunology
chemical_list: D016209:Interleukin-8; D008070:Lipopolysaccharides; D016328:NF-kappa B; D013682:Teichoic Acids; D014409:Tumor Necrosis Factor-alpha; C009900:lipoteichoic acid; C535150:MAPK1 protein, human; D019950:Mitogen-Activated Protein Kinase 1; D048052:Mitogen-Activated Protein Kinase 3
keywords: Apoptosis; Clostridium butyricum; HT-29 cells; Inflammatory response; Lipoteichoic acid; Staphylococcus aureus