Oral Bifidobacterium modulates intestinal immune inflammation in mice with food allergy.
OBJECTIVE
It is proposed that probiotics have a therapeutic effect on the treatment of immune disorders. However, the underlying mechanisms require clarification. The present study aimed to evaluate the effect of gavage-feeding Bifidobacteria on suppression of T helper 2 (Th2) pattern inflammation in the intestines of mice with food allergy.


METHODS
Mice were sensitized to ovalbumin to induce the intestinal Th2 pattern inflammation. Allergic mice were treated with or without Bifidobacteria via gavage-feeding. Th2 response, number of regulatory T cells (Treg) in the spleen and intestine, intestinal epithelial barrier function and bifidobacterial translocation were examined.


RESULTS
The results showed that serum-specific immunoglobulin E antibody and interleukin 4 (IL-4) were increased in allergic mice. Intestinal epithelial barrier function was impaired in allergic mice as shown by the increase in epithelial ion secretion and permeability to macromolecular protein horseradish peroxidase in Ussing chambers. Number of Treg was decreased in both spleen and intestines of allergic mice. Gavage-feeding Bifidobacteria significantly suppressed the skewed Th2 response and increased the number of Treg. Transient bifidobacterial translocation was observed in allergic mice.


CONCLUSIONS
Oral administration of Bifidobacteria has the capacity to suppress the skewed Th2 response in allergic mice, increasing the number of Treg and IL-10-positive cells and improve the impaired intestinal epithelial barrier function.
Zhang
Li-Li
LL
Department of Gastroenterology, the Second Affiliated Hospital of Zhengzhou University, Institute of Medical Microecology, Zhengzhou University, Zhengzhou, Henan, China.
Chen
Xiao
X
Zheng
Peng-Yuan
PY
Luo
Yu
Y
Lu
Gao-Feng
GF
Liu
Zhi-Qiang
ZQ
Huang
Huang
H
Yang
Ping-Chang
PC
D000284:Administration, Oral; D000818:Animals; D018988:Bacterial Translocation; D001644:Bifidobacterium / Q000235:genetics / Q000254:growth & development*; D003713:Dendritic Cells / Q000276:immunology / Q000382:microbiology; D004195:Disease Models, Animal; D004768:Enterotoxins; D005260:Female; D005512:Food Hypersensitivity / Q000276:immunology / Q000382:microbiology / Q000628:therapy*; D049452:Green Fluorescent Proteins / Q000235:genetics; D007073:Immunoglobulin E / Q000097:blood; D016753:Interleukin-10 / Q000097:blood; D015847:Interleukin-4 / Q000097:blood; D007413:Intestinal Mucosa / Q000276:immunology / Q000382:microbiology; D007422:Intestines / Q000276:immunology / Q000382:microbiology*; D007583:Jejunum / Q000276:immunology / Q000382:microbiology*; D051379:Mice; D008807:Mice, Inbred BALB C; D010047:Ovalbumin; D010539:Permeability; D019936:Probiotics / Q000008:administration & dosage*; D050378:T-Lymphocytes, Regulatory / Q000276:immunology / Q000382:microbiology; D018418:Th2 Cells / Q000276:immunology / Q000382:microbiology
D004768:Enterotoxins; D016753:Interleukin-10; D049452:Green Fluorescent Proteins; D015847:Interleukin-4; D007073:Immunoglobulin E; C031818:enterotoxin B, staphylococcal; D010047:Ovalbumin