Neonatal colonization of mice with LGG promotes intestinal development and decreases susceptibility to colitis in adulthood.
Development of the intestinal microbiota during early life serves as a key regulatory stage in establishing the host-microbial relationship. This symbiotic relationship contributes to developing host immunity and maintaining health throughout the life span. This study was to develop an approach to colonize conventionally raised mice with a model probiotic bacterium, Lactobacillus rhamnosus GG (LGG), and to determine the effects of LGG colonization on intestinal development and prevention of colitis in adulthood. LGG colonization in conventionally raised was established by administering LGG to pregnant mice starting at gestational day 18 and pups at postnatal days 1- 5. LGG colonization promoted bodyweight gain and increased diversity and richness of the colonic mucosa-associated microbiota before weaning. Intestinal epithelial cell proliferation, differentiation, tight junction formation, and mucosal IgA production were all significantly enhanced in LGG-colonized mice. Adult mice colonized with LGG showed increased IgA production and decreased susceptibility to intestinal injury and inflammation induced in the dextran sodium sulfate model of colitis. Thus, neonatal colonization of mice with LGG enhances intestinal functional maturation and IgA production and confers lifelong health consequences on protection from intestinal injury and inflammation. This strategy might be applied for benefiting health in the host.
Division of Gastroenterology, Hepatology and Nutrition, Department of Pediatrics, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
F
F
Yan
Division of Gastroenterology, Hepatology and Nutrition, Department of Pediatrics, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
L
L
Liu
Department of Gastroenterology and Hepatology, General Hospital, Tianjin Medical University, Tianjin, PR China.
H
H
Cao
Division of Endocrinology, Department of Pediatrics, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
D J
DJ
Moore
Department of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
M K
MK
Washington
Department of Gastroenterology and Hepatology, General Hospital, Tianjin Medical University, Tianjin, PR China.
B
B
Wang
Division of Gastroenterology, Departments of Medicine and Cancer Biology, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
R M
RM
Peek
Division of Gastroenterology, Hepatology and Nutrition, Department of Pediatrics, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
S A
SA
Acra
Departments of Pediatrics and Biochemistry and Molecular Biology, University of Southern California and Saban Research Institute of Children's Hospital Los Angeles, Los Angeles, California, USA.
D B
DB
Polk
D000818:Animals; D000831:Animals, Newborn; D049109:Cell Proliferation; D002478:Cells, Cultured; D003092:Colitis / Q000276:immunology* / Q000382:microbiology / Q000517:prevention & control; D016264:Dextran Sulfate; D004195:Disease Models, Animal; D005260:Female; D000069196:Gastrointestinal Microbiome / Q000276:immunology*; D006801:Humans; D007070:Immunoglobulin A / Q000378:metabolism*; D007413:Intestinal Mucosa / Q000276:immunology* / Q000382:microbiology / Q000473:pathology; D007422:Intestines / Q000382:microbiology / Q000502:physiology*; D052201:Lacticaseibacillus rhamnosus / Q000276:immunology*; D051379:Mice; D008810:Mice, Inbred C57BL; D011247:Pregnancy; D019936:Probiotics / Q000008:administration & dosage*; D013559:Symbiosis; D019108:Tight Junctions / Q000473:pathology
D007070:Immunoglobulin A; D016264:Dextran Sulfate