Role of intestinal Bifidobacterium pseudolongum in dietary fructo-oligosaccharide inhibition of 2,4-dinitrofluorobenzene-induced contact hypersensitivity in mice.
Strategies to manipulate the gut microbiota have been explored for preventing allergy development. We previously showed that dietary supplementation with fructo-oligosaccharide (FOS) reduced 2, 4-dinitrofluorobenzene (DNFB)-induced contact hypersensitivity (CHS) in BALB/c mice. Because the CHS response was negatively correlated with the number of faecal bifidobacteria, particularly Bifidobacterium pseudolongum, the present study aimed to examine whether oral administration of B. pseudolongum affects CHS response. Viable B. pseudolongum was successfully isolated from mouse faeces. Female BALB/c mice were fed a synthetic diet with or without FOS supplementation, and B. pseudolongum (2 x 10(7) cells) was administered daily throughout the experimental period. Two weeks after starting the test diets, mice received DNFB on the ear auricle twice at 7-d intervals. Conventional cultivation and molecular biological analyses based on 16S rRNA gene sequences showed that administration of FOS and B. pseudolongum resulted in higher excretion of viable bifidobacteria, mainly B. pseudolongum. Although dietary FOS reduced the CHS response as demonstrated by ear swelling, B. pseudolongum administration resulted in a reduction in the initial phase only of the CHS response. B. pseudolongum administration increased hapten-specific IgG1, while dietary FOS decreased IgG2a in sera. Administration of FOS and B. pseudolongum decreased interferon-gamma production and increased IL-10 production in cervical lymph node cells restimulated with hapten in vitro. We conclude that B. pseudolongum proliferation in the intestinal tract is partially responsible for the reduction in DNFB-induced CHS response by dietary supplementation with FOS in mice, which may be mediated by the modulation of antigen-induced cytokine production.
Sasajima
Naho
N
Laboratory of Gastrointestinal Physiology, Graduate School of Life Science, Hokkaido University, Sapporo 060-8589, Japan.
Ogasawara
Toru
T
Takemura
Naoki
N
Fujiwara
Reiko
R
Watanabe
Jun
J
Sonoyama
Kei
K
D000818:Animals; D001644:Bifidobacterium; D003877:Dermatitis, Contact / Q000178:diet therapy*; D004032:Diet; D004040:Dietary Carbohydrates / Q000494:pharmacology / Q000627:therapeutic use*; D019587:Dietary Supplements; D004139:Dinitrofluorobenzene; D004423:Ear; D004487:Edema / Q000517:prevention & control; D005243:Feces; D005260:Female; D006241:Haptens / Q000097:blood; D007074:Immunoglobulin G / Q000097:blood; D007371:Interferon-gamma / Q000096:biosynthesis; D016753:Interleukin-10 / Q000096:biosynthesis; D007422:Intestines / Q000382:microbiology*; D008198:Lymph Nodes / Q000378:metabolism; D051379:Mice; D008807:Mice, Inbred BALB C; D009844:Oligosaccharides / Q000494:pharmacology / Q000627:therapeutic use*; D056692:Prebiotics; D019936:Probiotics; D012336:RNA, Ribosomal, 16S
D004040:Dietary Carbohydrates; D006241:Haptens; D007074:Immunoglobulin G; D009844:Oligosaccharides; D056692:Prebiotics; D012336:RNA, Ribosomal, 16S; D016753:Interleukin-10; D007371:Interferon-gamma; D004139:Dinitrofluorobenzene