l-Malic acid (l-MA) enhanced Bifidobacterium breve Bb18 bile tolerance by 52.3% in vitro and synergistically alleviated DSS-induced colitis in mice, potentiating Bb18 colonization by 217.6% under inflammatory stress via gut microbiota-metabolite modulation.
Key Findings
Results
0.4% l-malic acid optimally enhanced Bb18 tolerance to glycodeoxycholic acid (GDCA) by 52.3% in vitro.
The concentration of 0.4% l-MA was identified as the optimal dose for enhancing bile tolerance.
The enhancement was specifically measured against glycodeoxycholic acid (GDCA).
Mechanisms included preserving membrane integrity, boosting energy metabolism, and upregulating bile salt efflux genes.
The authors describe this as 'promoting a multidimensional cellular adaptive response.'
Results
The combination of Bb18 and l-MA synergistically alleviated colon length shortening by 20.1% in DSS-induced colitis mice.
The study used a DSS-induced colitis mouse model.
Colon length shortening, a hallmark of colitis severity, was reduced by 20.1% with the combination treatment.
The combination also reduced inflammation and restored gut barrier integrity.
The effect was described as synergistic, implying greater efficacy than either component alone.
Results
l-MA potentiated Bb18 colonization under inflammatory stress by 217.6%.
This colonization enhancement was observed in the context of inflammatory stress in vivo.
The 217.6% increase indicates that l-MA substantially improved the ability of Bb18 to establish in the gut during colitis.
Improved colonization is described as a critical mechanism underlying the synergistic therapeutic effect.
This finding supports l-MA as a protective synbiotic partner for probiotic delivery under disease conditions.
Results
The Bb18 and l-MA combination simultaneously modulated gut microbiota composition and increased barrier-protective metabolites linked to inflammation resolution.
The combination treatment affected both the gut microbial community structure and metabolite profiles.
Increased barrier-protective metabolites were mechanistically linked to inflammation resolution.
This dual modulation of microbiota and metabolites represents a proposed mechanism of action for the synergistic effect.
The findings support a gut microbiota-metabolite modulation pathway as central to the therapeutic efficacy.
Conclusions
l-MA functions as a protective synbiotic partner for Bb18, offering a novel combinatorial strategy for probiotic-enhanced colitis management.
The study establishes l-MA in the role of a synbiotic component rather than just a prebiotics or food additive.
The protective effects were demonstrated both in vitro (bile tolerance) and in vivo (colonization and anti-inflammatory effects).
The combination strategy addresses the challenge of probiotic survival and colonization under inflammatory conditions.
Authors propose this as 'a novel combinatorial strategy for probiotic-enhanced colitis management.'
Tong Y, Li L, Liu X, Song J, Yang R, Feng S. (2026). l-Malic Acid Potentiates Bifidobacterium breve Bb18 Tolerance and Synergistically Ameliorates Colitis via Gut Microbiota-Metabolite Modulation.. Journal of agricultural and food chemistry. https://doi.org/10.1021/acs.jafc.5c15404