title: Bacteriocins from lactic acid bacteria increases tumor necrosis factor-alpha expression in a rat kidney model of chronic rejection.
abstract: Chronic allograft dysfunction is the primary cause of graft loss after the first posttransplantation year. Bacteriocins are biologically active proteins exhibiting antimicrobial properties against other bacterial species, which are usually closely related to the producer organism. The objective of our study was to determine whether lactic acid bacterial bacteriocins were associated with tumor necrosis factor (TNF)-alpha observed in a rat kidney model of chronic rejection. Using a kidney model of chronic rejection in the rat, we administered cyclosporine (CsA) immunosuppression (5 mg/kg/d). One group of animals was treated with bacteriocins, and the other was left untreated. Grafts were harvested after transplantation for standard histological studies. The expression of TNF-alpha was demonstrated using immunohistochemistry of frozen sections of the grafts. We observed a greater increase in the expression of TNF-alpha among the group treated with bacteriocins compared with the untreated group. These results showed that lactic acid bacterial bacteriocins were associated with TNF-alpha in our kidney graft model.
authors.affiliation: Institute of Plant Protection and Microbiology, Zhejiang Academy of Agricultural Sciences, Hangzhou, China.
authors.forename: L H
authors.initials: LH
authors.lastname: Zhu
authors.forename: C
authors.initials: C
authors.lastname: Li
authors.forename: J A
authors.initials: JA
authors.lastname: Wu
authors.forename: J G
authors.initials: JG
authors.lastname: Liang
authors.forename: Y F
authors.initials: YF
authors.lastname: Shi
mesh_terms: D000818:Animals; D001430:Bacteriocins / Q000302:isolation & purification / Q000494:pharmacology*; D002908:Chronic Disease; D004730:Endothelium, Vascular / Q000187:drug effects / Q000503:physiopathology; D006084:Graft Rejection / Q000276:immunology / Q000382:microbiology* / Q000503:physiopathology; D007165:Immunosuppression Therapy; D007249:Inflammation / Q000503:physiopathology; D016030:Kidney Transplantation / Q000473:pathology* / Q000502:physiology; D007777:Lactobacillaceae / Q000235:genetics* / Q000276:immunology; D023421:Models, Animal; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000503:physiopathology; D051381:Rats; D011914:Rats, Inbred BN; D011919:Rats, Inbred Strains; D014184:Transplantation, Homologous; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics*
chemical_list: D001430:Bacteriocins; D014409:Tumor Necrosis Factor-alpha