title: Influence of orally fed a select mixture of Bacillus probiotics on intestinal T-cell migration in weaned MUC4 resistant pigs following Escherichia coli challenge.
abstract: Efficient strategies for treating enteritis caused by F4(+) enterotoxigenic Escherichia coli (ETEC)/verocytotoxigenic Escherichia coli (VTEC)/enteropathogenic E. coli (EPEC) in mucin 4 resistant (MUC4 RR; supposed to be F4ab/ac receptor-negative [F4ab/acR(-)]) pigs remain elusive. A low (3.9 × 10(8) CFU/day) or high (7.8 × 10(8) CFU/day) dose of Bacillus licheniformis and Bacillus subtilis spore mixture (BLS-mix) was orally administered to MUC4 RR piglets for 1 week before F4(+) ETEC/VTEC/EPEC challenge. Orally fed BLS-mix upregulated the expression of TLR4, NOD2, iNOS, IL-8, and IL-22 mRNAs in the small intestine of pigs challenged with E. coli. Expression of chemokine CCL28 and its receptor CCR10 mRNAs was upregulated in the jejunum of pigs pretreated with high-dose BLS-mix. Low-dose BLS-mix pretreatment induced an increase in the proportion of peripheral blood CD4(-)CD8(-) T-cell subpopulations and high-dose BLS-mix induced the expansion of CD4(-)CD8(-) T cells in the inflamed intestine. Immunostaining revealed that considerable IL-7Rα-expressing cells accumulated at the lamina propria of the inflamed intestines after E. coli challenge, even in pigs pretreated with either low- or high-dose BLS-mix, although Western blot analysis of IL-7Rα expression in the intestinal mucosa did not show any change. Our data indicate that oral administration of the probiotic BLS-mix partially ameliorates E. coli-induced enteritis through facilitating upregulation of intestinal IL-22 and IκBα expression, and preventing loss of intestinal epithelial barrier integrity via elevating ZO-1 expression. However, IL-22 also elicits an inflammatory response in inflamed intestines as a result of infection with enteropathogenic bacteria.
authors.affiliation: College of Veterinary Medicine, China Agricultural University, Beijing, 100193, China.
authors.forename: Gui-Yan
authors.initials: GY
authors.lastname: Yang
authors.affiliation: College of Veterinary Medicine, China Agricultural University, Beijing, 100193, China.
authors.forename: Yao-Hong
authors.initials: YH
authors.lastname: Zhu
authors.affiliation: College of Veterinary Medicine, China Agricultural University, Beijing, 100193, China.
authors.forename: Wei
authors.initials: W
authors.lastname: Zhang
authors.affiliation: College of Veterinary Medicine, China Agricultural University, Beijing, 100193, China.
authors.forename: Dong
authors.initials: D
authors.lastname: Zhou
authors.affiliation: College of Veterinary Medicine, China Agricultural University, Beijing, 100193, China.
authors.forename: Cong-Cong
authors.initials: CC
authors.lastname: Zhai
authors.affiliation: College of Veterinary Medicine, China Agricultural University, Beijing, 100193, China. jiufeng_wang@hotmail.com.
authors.forename: Jiu-Feng
authors.initials: JF
authors.lastname: Wang
mesh_terms: D000818:Animals; D001407:Bacillus / Q000276:immunology*; D018791:CD4 Lymphocyte Count / Q000662:veterinary; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology; D060467:Disease Resistance / Q000276:immunology; D054307:Enterotoxigenic Escherichia coli / Q000276:immunology; D004927:Escherichia coli Infections / Q000276:immunology / Q000517:prevention & control / Q000662:veterinary*; D005260:Female; D007378:Interleukins / Q000378:metabolism; D007413:Intestinal Mucosa / Q000378:metabolism; D007422:Intestines / Q000276:immunology* / Q000382:microbiology; D008297:Male; D000072000:NF-KappaB Inhibitor alpha / Q000378:metabolism; D019936:Probiotics / Q000627:therapeutic use*; D013552:Swine; D013553:Swine Diseases / Q000276:immunology* / Q000382:microbiology; D013601:T-Lymphocytes / Q000276:immunology*
chemical_list: D007378:Interleukins; D000072000:NF-KappaB Inhibitor alpha