Bifidobacterium breve HH079 alleviates early-life antibiotic-exposed colon dysbiosis in mice by restoring the gut microbiota and gut barrier function

Antibiotic exposure in early life disrupts gut microbiota development in infants, which could result in intestinal dysfunction. This study mimicked early-life antibiotic exposure in mice by administering antibiotic water to lactating dams, and investigated the effects of a new strain of Bifidobacter...

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Published inFood & function Vol. 16; no. 10; pp. 3833 - 3847
Main Authors Gu, Zhipeng, Lu, Zerong, Wu, Jian-yong, Xie, Zhuqing, Hu, Ruibiao, Huang, Qiang, Liu, Feitong, Zhang, Bin
Format Journal Article
LanguageEnglish
Published England Royal Society of Chemistry 19.05.2025
Subjects
Online AccessGet full text
ISSN2042-6496
2042-650X
2042-650X
DOI10.1039/D5FO00535C

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Abstract Antibiotic exposure in early life disrupts gut microbiota development in infants, which could result in intestinal dysfunction. This study mimicked early-life antibiotic exposure in mice by administering antibiotic water to lactating dams, and investigated the effects of a new strain of Bifidobacterium breve HH079 ( B. breve HH079) on intestinal dysbiosis associated with early-life antibiotic exposure in pups. The results showed that B. breve HH079 treatment inhibited the proliferation of Pseudomonas and Morganella after antibiotic exposure, but promoted the abundance of Bifidobacterium and Bacteroides and acetate production. Concomitantly, the B. breve HH079 administration resulted in decreased M1 gene ( Cd86 ) and protein (TNF-α, IL-1β, LBP and iNOS) expression and increased M2 macrophage marker ( Cd206 , IL-10 and Arg1) expression in the colonic macrophages of antibiotic-exposed pups, probably by inhibiting the TLR4/NF-κB pathway. Moreover, there was increased intestinal epithelial tight junction protein (Cldn1 and Ocln) expression and the transcription of marker gene ( Lyz2 , Igha and Reg3β ) normalization involved in innate immunity. The results suggested that the new B. breve HH079 strain could alleviate early-life antibiotic-induced colon dysbiosis by regulating the gut microbiota and promoting acetate production and the subsequent M2 macrophage polarization to recover gut health.
AbstractList Antibiotic exposure in early life disrupts gut microbiota development in infants, which could result in intestinal dysfunction. This study mimicked early-life antibiotic exposure in mice by administering antibiotic water to lactating dams, and investigated the effects of a new strain of Bifidobacterium breve HH079 (B. breve HH079) on intestinal dysbiosis associated with early-life antibiotic exposure in pups. The results showed that B. breve HH079 treatment inhibited the proliferation of Pseudomonas and Morganella after antibiotic exposure, but promoted the abundance of Bifidobacterium and Bacteroides and acetate production. Concomitantly, the B. breve HH079 administration resulted in decreased M1 gene (Cd86) and protein (TNF-α, IL-1β, LBP and iNOS) expression and increased M2 macrophage marker (Cd206, IL-10 and Arg1) expression in the colonic macrophages of antibiotic-exposed pups, probably by inhibiting the TLR4/NF-κB pathway. Moreover, there was increased intestinal epithelial tight junction protein (Cldn1 and Ocln) expression and the transcription of marker gene (Lyz2, Igha and Reg3β) normalization involved in innate immunity. The results suggested that the new B. breve HH079 strain could alleviate early-life antibiotic-induced colon dysbiosis by regulating the gut microbiota and promoting acetate production and the subsequent M2 macrophage polarization to recover gut health.Antibiotic exposure in early life disrupts gut microbiota development in infants, which could result in intestinal dysfunction. This study mimicked early-life antibiotic exposure in mice by administering antibiotic water to lactating dams, and investigated the effects of a new strain of Bifidobacterium breve HH079 (B. breve HH079) on intestinal dysbiosis associated with early-life antibiotic exposure in pups. The results showed that B. breve HH079 treatment inhibited the proliferation of Pseudomonas and Morganella after antibiotic exposure, but promoted the abundance of Bifidobacterium and Bacteroides and acetate production. Concomitantly, the B. breve HH079 administration resulted in decreased M1 gene (Cd86) and protein (TNF-α, IL-1β, LBP and iNOS) expression and increased M2 macrophage marker (Cd206, IL-10 and Arg1) expression in the colonic macrophages of antibiotic-exposed pups, probably by inhibiting the TLR4/NF-κB pathway. Moreover, there was increased intestinal epithelial tight junction protein (Cldn1 and Ocln) expression and the transcription of marker gene (Lyz2, Igha and Reg3β) normalization involved in innate immunity. The results suggested that the new B. breve HH079 strain could alleviate early-life antibiotic-induced colon dysbiosis by regulating the gut microbiota and promoting acetate production and the subsequent M2 macrophage polarization to recover gut health.
Antibiotic exposure in early life disrupts gut microbiota development in infants, which could result in intestinal dysfunction. This study mimicked early-life antibiotic exposure in mice by administering antibiotic water to lactating dams, and investigated the effects of a new strain of HH079 ( HH079) on intestinal dysbiosis associated with early-life antibiotic exposure in pups. The results showed that HH079 treatment inhibited the proliferation of and after antibiotic exposure, but promoted the abundance of and and acetate production. Concomitantly, the HH079 administration resulted in decreased M1 gene ( ) and protein (TNF-α, IL-1β, LBP and iNOS) expression and increased M2 macrophage marker ( , IL-10 and Arg1) expression in the colonic macrophages of antibiotic-exposed pups, probably by inhibiting the TLR4/NF-κB pathway. Moreover, there was increased intestinal epithelial tight junction protein (Cldn1 and Ocln) expression and the transcription of marker gene ( , and ) normalization involved in innate immunity. The results suggested that the new HH079 strain could alleviate early-life antibiotic-induced colon dysbiosis by regulating the gut microbiota and promoting acetate production and the subsequent M2 macrophage polarization to recover gut health.
Antibiotic exposure in early life disrupts gut microbiota development in infants, which could result in intestinal dysfunction. This study mimicked early-life antibiotic exposure in mice by administering antibiotic water to lactating dams, and investigated the effects of a new strain of Bifidobacterium breve HH079 (B. breve HH079) on intestinal dysbiosis associated with early-life antibiotic exposure in pups. The results showed that B. breve HH079 treatment inhibited the proliferation of Pseudomonas and Morganella after antibiotic exposure, but promoted the abundance of Bifidobacterium and Bacteroides and acetate production. Concomitantly, the B. breve HH079 administration resulted in decreased M1 gene (Cd86) and protein (TNF-α, IL-1β, LBP and iNOS) expression and increased M2 macrophage marker (Cd206, IL-10 and Arg1) expression in the colonic macrophages of antibiotic-exposed pups, probably by inhibiting the TLR4/NF-κB pathway. Moreover, there was increased intestinal epithelial tight junction protein (Cldn1 and Ocln) expression and the transcription of marker gene (Lyz2, Igha and Reg3β) normalization involved in innate immunity. The results suggested that the new B. breve HH079 strain could alleviate early-life antibiotic-induced colon dysbiosis by regulating the gut microbiota and promoting acetate production and the subsequent M2 macrophage polarization to recover gut health.
Author Wu, Jian-yong
Huang, Qiang
Lu, Zerong
Zhang, Bin
Gu, Zhipeng
Hu, Ruibiao
Liu, Feitong
Xie, Zhuqing
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Snippet Antibiotic exposure in early life disrupts gut microbiota development in infants, which could result in intestinal dysfunction. This study mimicked early-life...
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SubjectTerms Acetates - metabolism
Acetic acid
Ampicillin - pharmacology
Animals
Anti-Bacterial Agents - chemistry
Anti-Bacterial Agents - pharmacology
Antibiotics
Bifidobacterium breve
Bifidobacterium breve - drug effects
CD86 antigen
Colon
Colon - drug effects
Colon - metabolism
Colon - microbiology
Colon - pathology
Digestive system
Dysbacteriosis
Dysbiosis - drug therapy
Dysbiosis - microbiology
Exposure
Gastrointestinal Microbiome - drug effects
Gastrointestinal tract
Gene Expression Regulation, Bacterial - drug effects
Innate immunity
Innate Immunity Recognition
Intestinal Barrier Function - drug effects
Intestinal microflora
Intestine
Juveniles
Macrophages
Macrophages - drug effects
Macrophages - microbiology
Mice
Mice, Inbred C57BL
Microbiota
Microorganisms
Neomycin - pharmacology
NF-kappa B - metabolism
NF-κB protein
Nitric-oxide synthase
Proteins
Signal Transduction - drug effects
TLR4 protein
Toll-like receptors
Tumor necrosis factor-α
Title Bifidobacterium breve HH079 alleviates early-life antibiotic-exposed colon dysbiosis in mice by restoring the gut microbiota and gut barrier function
URI https://www.ncbi.nlm.nih.gov/pubmed/40143684
https://www.proquest.com/docview/3205518206
https://www.proquest.com/docview/3181820944
Volume 16
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