Letters in applied microbiology · 2008
Cell wall fraction of Enterococcus hirae ameliorates TNF-alpha-induced barrier impairment in the human epithelial tight junction.
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Miyauchi E, Morita H, Okuda J, Sashihara T, Shimizu M, Tanabe S
Аннотация
AIMS: The evaluation of the effects of Enterococcus hirae, an intestinal bacterium in the adjacent mucosa (mucosal bacterium), on tumour necrosis factor-alpha (TNF-alpha)-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 9790(T) suppressed the TNF-alpha-induced barrier impairment and increase in interleukin-8 (IL-8) secretion, but lipase- and mutanolysin-treated E. hirae ATCC 9790(T) did not have these effects. It was demonstrated that lipoteichoic acid (LTA) from E. hirae ATCC 9790(T) is responsible for Caco-2 cells' recovery from TNF-alpha-induced impairments. In addition, Caco-2 cells had the same response to Toll-like receptor 2 (TLR2) ligand, Pam(3)Cys-Ser-(Lys)(4) as they did to LTA. Increased expression of zonula occludens-1 was observed by the addition of E. hirae ATCC 9790(T) to TNF-alpha-treated Caco-2 cells, and decreased expression of myosin light chain kinase was observed by the addition of LTA and Pam(3)Cys-Ser-(Lys)(4); this, in turn, led to barrier enforcement.
CONCLUSIONS: Enterococcus hirae ATCC 9790(T) 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.
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 9790(T) suppressed the TNF-alpha-induced barrier impairment and increase in interleukin-8 (IL-8) secretion, but lipase- and mutanolysin-treated E. hirae ATCC 9790(T) did not have these effects. It was demonstrated that lipoteichoic acid (LTA) from E. hirae ATCC 9790(T) is responsible for Caco-2 cells' recovery from TNF-alpha-induced impairments. In addition, Caco-2 cells had the same response to Toll-like receptor 2 (TLR2) ligand, Pam(3)Cys-Ser-(Lys)(4) as they did to LTA. Increased expression of zonula occludens-1 was observed by the addition of E. hirae ATCC 9790(T) to TNF-alpha-treated Caco-2 cells, and decreased expression of myosin light chain kinase was observed by the addition of LTA and Pam(3)Cys-Ser-(Lys)(4); this, in turn, led to barrier enforcement.
CONCLUSIONS: Enterococcus hirae ATCC 9790(T) 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.