title: Oral administration of Bifidobacterium longum culture condensate in a diet-restricted murine peritonitis model enhances polymorphonuclear neutrophil recruitment into the local inflammatory site.
abstract: Dietary restriction impairs polymorphonuclear neutrophil (PMN) recruitment into the local inflammatory site, resulting in susceptibility to infection. Probiotics enhance host immunity via conditioning host intestinal microflora. Oral administration of Bifidobacterium longum culture condensate (BCC) in a diet-restricted murine peritonitis model may enhance PMN recruitment into the inflammatory site. Male ICR mice (n = 40) were assigned in equal numbers to control or BCC groups and subjected to 75% restricted food intake for 7 d. During dietary restriction, controls received only standard mouse chow, whereas the BCC group received standard mouse chow containing 1% BCC. Mice were killed before (0 h) or after (2 or 4 h) intraperitoneal glycogen injection. Peritoneal lavage fluid and exudative cells were recovered by peritoneal lavage. Peritoneal exudative cell number was counted. Tumor necrosis factor-alpha, interleukin-6, macrophage inflammatory protein-2, and interleukin-10 concentrations in peritoneal lavage fluid were determined by enzyme-linked immunosorbent assay. CD11b, CD18, CD31, and CD62L expressions on circulating PMNs were measured by flow cytometry. Oral BCC administration upregulated PMN recruitment into the peritoneal cavity and increased peritoneal fluid cytokine concentrations as well as CD18 and CD62L expressions on circulating PMNs during glycogen-induced peritonitis. Oral BCC administration in a diet-restricted murine peritonitis model augmented PMN recruitment into the inflammatory site by upregulating cytokine concentrations in the local inflammatory site and adhesion molecule expression on circulating PMNs. Oral BCC administration may be a favorable modality for improving dietary restriction-induced host immunosuppression.
authors.affiliation: Department of Surgery, Faculty of Medicine, Tokyo, Japan. hidemura-tky@umin.ac.jp
authors.forename: Akio
authors.initials: A
authors.lastname: Hidemura
authors.forename: Hideaki
authors.initials: H
authors.lastname: Saito
authors.forename: Kazuhiko
authors.initials: K
authors.lastname: Fukatsu
authors.forename: Takeaki
authors.initials: T
authors.lastname: Matsuda
authors.forename: Joji
authors.initials: J
authors.lastname: Kitayama
authors.forename: Shigeo
authors.initials: S
authors.lastname: Ikeda
authors.forename: Woodae
authors.initials: W
authors.lastname: Kang
authors.forename: Hirokazu
authors.initials: H
authors.lastname: Nagawa
mesh_terms: D000284:Administration, Oral; D000818:Animals; D015703:Antigens, CD / Q000096:biosynthesis; D001202:Ascitic Fluid / Q000276:immunology; D001644:Bifidobacterium / Q000502:physiology*; D018925:Chemokines / Q000378:metabolism; D004038:Diet, Reducing; D004195:Disease Models, Animal; D005434:Flow Cytometry; D007249:Inflammation / Q000150:complications / Q000276:immunology; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D009504:Neutrophils / Q000276:immunology / Q000502:physiology*; D009748:Nutrition Disorders / Q000276:immunology; D010529:Peritoneal Cavity / Q000166:cytology; D010538:Peritonitis / Q000139:chemically induced / Q000276:immunology*; D019936:Probiotics / Q000008:administration & dosage*; D011897:Random Allocation; D013047:Specific Pathogen-Free Organisms
chemical_list: D015703:Antigens, CD; D018925:Chemokines