Mechanism underlying prolongevity induced by bifidobacteria in Caenorhabditis elegans

Abstract

Lactobacilli and bifidobacteria are probiotic bacteria that modify host defense systems and have the ability to extend the lifespan of the nematode Caenorhabditis elegans. Here, we attempted to elucidate the mechanism by which bifidobacteria prolong the lifespan of C. elegans. When the nematode was fed Bifidobacterium infantis (BI) mixed at various ratios with the standard food bacterium Escherichia coli strain OP50 (OP), the mean lifespan of worms was extended in a dose-dependent manner. Worms fed BI displayed higher locomotion and produced more offspring than control worms. The growth curves of nematodes were similar regardless of the amount of BI mixed with OP, suggesting that BI did not induce prolongevity effects through caloric restriction. Notably, feeding worms the cell wall fraction of BI alone was sufficient to promote prolongevity. The accumulation of protein carbonyls and lipofuscin, a biochemical marker of aging, was also lower in worms fed BI; however, the worms displayed similar susceptibility to heat, hydrogen peroxide, and paraquat, an inducer of free radicals, as the control worms. As a result of BI feeding, loss-of-function mutants of daf-16, jnk-1, aak-2, tol-1, and tir-1 exhibited a longer lifespan than OP-fed control worms, but BI failed to extend the lifespan of pmk-1, skn-1, and vhp-1 mutants. As skn-1 induces phase 2 detoxification enzymes, our findings suggest that cell wall components of bifidobacteria increase the average lifespan of C. elegans via activation of skn-1, regulated by the p38 MAPK pathway, but not by general activation of the host defense system via DAF-16.

Lactobacillus zeae Protects Caenorhabditis elegans from Enterotoxigenic Escherichia coli-Caused Death by Inhibiting Enterotoxin Gene Expression of the Pathogen

“…These pathways include: 1) P38-MAPK pathway, 2) TGF-β pathway, and 3) Insulin/IGF-like pathway. Lactobacillus can also induce C. elegans ’s host response [43], [44]. In the present study, L. zeae LB1 was able to effectively prevent C. elegans from death caused by ETEC JG280 or individual enterotoxin clones (Table 1, Fig.…”

Dietary and microbiome factors determine longevity in Caenorhabditis elegans

“…According to these authors and in agreement with our own results, TOL-1 has a direct role in the immune response to certain gram negative bacteria. It was reported that worms fed the gram positive Bifidobacterium infantis lived longer than E. coli fed worms, and that tol-1 mutant worms lived longer on B. infantis than WT worms [57]. We speculate that TOL-1 functions to protect C. elegans against gram negative specific factors, but that the activity of this protection system might be detrimental as when TOL-1 is not functional and the gram negative threat is not present (worms are fed gram positive bacteria), worms live longer than WT worms.…”

Commensals, probiotics and pathogens in theCaenorhabditis elegansmodel

“…A study examining the effect of Bifidobacterium infantis on C. elegans lifespan found a modest dose‐dependent lifespan extension when B. infantis was added to OP50 (Komura et al ., ). The authors also report an extension in healthspan of worms fed B. infantis , defined by locomotion and co‐ordination.…”

“…2A). Several studies Fasseas et al, 2013;Komura et al, 2013;MacNeil et al, 2013) have ruled out the involvement of DAF-16 in probiotic-mediated lifespan extension, indicating that there are multiple independent pathways affecting C. elegans longevity.…”