TY - JOUR
T1 - Cell wall fraction of Enterococcus hirae ameliorates TNF-α-induced barrier impairment in the human epithelial tight junction
AU - Miyauchi, E.
AU - Morita, H.
AU - Okuda, J.
AU - Sashihara, T.
AU - Shimizu, M.
AU - Tanabe, S.
N1 - Copyright:
Copyright 2008 Elsevier B.V., All rights reserved.
PY - 2008/4
Y1 - 2008/4
N2 - Aims: The evaluation of the effects of Enterococcus hirae, an intestinal bacterium in the adjacent mucosa (mucosal bacterium), on tumour necrosis factor-alpha (TNF-α)-induced barrier impairment in human epithelial Caco-2 cells. Methods and Results: The filter-grown Caco-2 monolayers were used as an intestinal epithelial model system. In Caco-2 cells, heat-killed E. hirae ATCC 9790T suppressed the TNF-α-induced barrier impairment and increase in interleukin-8 (IL-8) secretion, but lipase- and mutanolysin-treated E. hirae ATCC 9790T did not have these effects. It was demonstrated that lipoteichoic acid (LTA) from E. hirae ATCC 9790T is responsible for Caco-2 cells' recovery from TNF-α-induced impairments. In addition, Caco-2 cells had the same response to Toll-like receptor 2 (TLR2) ligand, Pam3Cys-Ser-(Lys)4 as they did to LTA. Increased expression of zonula occludens-1 was observed by the addition of E. hirae ATCC 9790T to TNF-α-treated Caco-2 cells, and decreased expression of myosin light chain kinase was observed by the addition of LTA and Pam 3Cys-Ser-(Lys)4; this, in turn, led to barrier enforcement. Conclusions: Enterococcus hirae ATCC 9790T cell wall fractions, such as LTA, protect against intestinal impairment by regulation of epithelial tight junction via TLR2 signalling. Significance and Impact of the Study: Enterococcus hirae could be useful in the treatment of inflammatory bowel disease, as well as other intestinal disorders.
AB - Aims: The evaluation of the effects of Enterococcus hirae, an intestinal bacterium in the adjacent mucosa (mucosal bacterium), on tumour necrosis factor-alpha (TNF-α)-induced barrier impairment in human epithelial Caco-2 cells. Methods and Results: The filter-grown Caco-2 monolayers were used as an intestinal epithelial model system. In Caco-2 cells, heat-killed E. hirae ATCC 9790T suppressed the TNF-α-induced barrier impairment and increase in interleukin-8 (IL-8) secretion, but lipase- and mutanolysin-treated E. hirae ATCC 9790T did not have these effects. It was demonstrated that lipoteichoic acid (LTA) from E. hirae ATCC 9790T is responsible for Caco-2 cells' recovery from TNF-α-induced impairments. In addition, Caco-2 cells had the same response to Toll-like receptor 2 (TLR2) ligand, Pam3Cys-Ser-(Lys)4 as they did to LTA. Increased expression of zonula occludens-1 was observed by the addition of E. hirae ATCC 9790T to TNF-α-treated Caco-2 cells, and decreased expression of myosin light chain kinase was observed by the addition of LTA and Pam 3Cys-Ser-(Lys)4; this, in turn, led to barrier enforcement. Conclusions: Enterococcus hirae ATCC 9790T cell wall fractions, such as LTA, protect against intestinal impairment by regulation of epithelial tight junction via TLR2 signalling. Significance and Impact of the Study: Enterococcus hirae could be useful in the treatment of inflammatory bowel disease, as well as other intestinal disorders.
KW - Caco-2
KW - Enterococcus hirae
KW - Inflammatory bowel disease
KW - Lipoteichoic acid
KW - Myosin light chain kinase
KW - Tight junction
KW - Zonula occludens-1
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U2 - 10.1111/j.1472-765X.2008.02332.x
DO - 10.1111/j.1472-765X.2008.02332.x
M3 - Article
C2 - 18298454
AN - SCOPUS:41049088858
VL - 46
SP - 469
EP - 476
JO - Letters in Applied Microbiology
JF - Letters in Applied Microbiology
SN - 0266-8254
IS - 4
ER -