Toll-like receptor-2-activating bifidobacteria strains diferentially regulate inflammatory cytokines in the porcine intestinal epithelial cell culture system: finding new anti-inflammatory immunobiotics

HITOMI FUJIE; JULIO VILLENA; MASANORI TOHNO; KYOKO MORIE; TOMOYUKI SHIMAZU; HISASHI ASO; YOSHIHITO SUDA; TAKESHI SHIMOSATO; NORIYUKI IWABUCHI; JIN-ZHONG XIAO; TOMOKO YAESHIMA; KEIJI IWATSUKI; TADAO SAITO; MUNEO NUMASAKI; HARUKI KITAZAWA

FEMS IMMUNOLOGY AND MEDICAL MICROBIOLOGY

WILEY-BLACKWELL PUBLISHING, INC

Año: 2011 vol. 63 p. 129 - 139

0928-8244

A total of 23 strains of bifidobacteria taxonomically belonging to five species were tested for their potent immunomodulatory effect using a combination of two methods: the NF-kB-reporter assay using a toll-like receptor 2-expressing transfectant (HEKpTLR2 system) and the mitogenic assay using porcine Peyer’s patches immuno- competent cells. Among the four preselected strains from different immunomodula- tory groups, Bifidobacterium breve MCC-117 was able to efficiently modulate the inflammatory response triggered by enterotoxigenic Escherichia coli (ETEC) in a porcine intestinal epithelial (PIE) cell line. Moreover, using PIE cells and swine Peyer’s patches immunocompetent cell co-culture system, we demonstrated that the immunoregulatory effect of B. breve MCC-117 was related to the capacity of the strain to influence PIE and immune cell interactions, leading to the stimulation of regulatory T cells. The results suggested that bifidobacteria that express high activity in both the HEKpTLR2 and the mitogenic assays may behave like potential anti- inflammatory strains. The combination of the HEKpTLR2 system, the evaluation of mitogenic activity and PIE cells will be of value for the development of new immunologically functional foods and feeds that could prevent inflammatory intestinal disorders. Although our findings should be proven in appropriate experi- ments in vivo, the results of the present work provide a scientific rationale for the use of B. breve MCC-117 to prevent ETEC-induced intestinal inflammation.