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GH136-encoding gene (perB) is involved in gut colonization and persistence by Bifidobacterium bifidum PRL2010
Sonia Mirjam Rizzo1, Laura Maria Vergna1, Giulia Alessandri1
1Laboratory of Probiogenomics, Department of Chemistry, Life Sciences and Environmental Sustainability, University of Parma, Parma, Italy.
Insights
The perB gene aids Bifidobacterium bifidum in adhering to mucin and persisting in the gut. Inactivating perB reduces its ability to grow on mucin and colonize the rodent gut.
Area of Science:
- Microbiology
- Genomics
- Gastroenterology
Background:
- Bifidobacteria are crucial gut commensals, important from birth through old age.
- Genes for adhesion and carbohydrate degradation contribute to bifidobacterial gut persistence.
- The perB gene, encoding a mucin-degrading enzyme (GH136 family), is a recent focus for gut colonization.
Purpose of the Study:
- To investigate the functional role of the perB gene in Bifidobacterium bifidum gut persistence.
- To characterize the mucin-degrading activity and adhesion properties associated with perB.
Main Methods:
- Comparative genomic analysis to identify perB homologues in bifidobacterial species.
- In vitro experiments assessing mucin-mediated growth and adhesion to human intestinal cells using a perB mutant.
- In vivo colonization assay in a rodent model.
Main Results:
- PerB homologues are present in specific human-gut-colonizing bifidobacterial species.
- perB inactivation in B. bifidum PRL2010 significantly impaired growth on mucin and adhesion to intestinal cells.
- The perB-deficient mutant showed reduced persistence in the rodent gut model.
Conclusions:
- The perB gene is a key determinant for Bifidobacterium bifidum's ability to utilize mucin and adhere to the gut lining.
- PerB plays a significant role in the in vivo persistence of B. bifidum in the intestinal environment.
Abstract:
Bifidobacteria are commensal microorganisms that typically inhabit the mammalian gut, including that of humans. As they may be vertically transmitted, they commonly colonize the human intestine from the very first day following birth and may persist until adulthood and old age, although generally at a reduced relative abundance and prevalence compared to infancy. The ability of bifidobacteria to persist in the human intestinal environment has been attributed to genes involved in adhesion to epithelial cells and the encoding of complex carbohydrate-degrading enzymes. Recently, a putative mucin-degrading glycosyl hydrolase belonging to the GH136 family and encoded by the perB gene has been implicated in gut persistence of certain bifidobacterial strains. In the current study, to better characterize the function of this gene, a comparative genomic analysis was performed, revealing the presence of perB homologues in just eight bifidobacterial species known to colonize the human gut, including Bifidobacterium bifidum and Bifidobacterium longum subsp. longum strains, or in non-human primates. Mucin-mediated growth and adhesion to human intestinal cells, in addition to a rodent model colonization assay, were performed using B. bifidum PRL2010 as a perB prototype and its isogenic perB-insertion mutant. These results demonstrate that perB inactivation reduces the ability of B. bifidum PRL2010 to grow on and adhere to mucin, as well as to persist in the rodent gut niche. These results corroborate the notion that the perB gene is one of the genetic determinants involved in the persistence of B. bifidum PRL2010 in the human gut.
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