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Abstract

The invasion of pathogens causes a disruption of the gut homeostasis. Innate immune responses and those triggered by endogenous microbiota form the first line of defence in our body. Pathogens often successfully overcome the resistances offered, calling for therapeutic intervention. Conventional strategy involving antibiotics might eradicate pathogens, but often leave the gut uncolonised and susceptible to recurrences. Probiotic supplements are useful alternatives. Bifidobacterium is one of widely studied probiotic genus, effective in restoring gut homeostasis. Mechanisms of probiotic action of bifidobacteria are several, often with strain-specificity. Analysis of streamlined literature reports reveal that although most studies report the probiotic aspect of bifidobacteria, sporadic documented contradictory results exist, challenging its therapeutic application and prompting studies to unambiguously establish the strain-associated probiotic activity and negate adverse effects prior to its clinical administration. Multi-strain/combinatorial therapy possibly relies on a combination of underlying operating mechanisms, each contributing towards enhanced probiotic efficacy, understanding which could help in developing customised formulations against targeted pathogens. Bifidogenic activity is also mediated by surface-associated structural components such as exopolysaccharides, lipoteichoic acids along with metabolites and bifidocins. This highlights scope for developing advanced structural therapeutic strategy which might be pivotal in replacing intact cell probiotics therapy.

Keywords: Adverse effects; Clinical application; Combinatorial therapy; Gut microbiome; Immunomodulatory effect; Pathogen protection.

Research Insights

SupplementHealth OutcomeEffect TypeEffect Size
BifidobacteriumImproved Gut HomeostasisBeneficial
Moderate
BifidobacteriumImproved Probiotic EfficiencyBeneficial
Moderate
BifidobacteriumIncreased Adverse EffectsHarmful
Small
BifidobacteriumReduced Pathogen ResistanceBeneficial
Moderate
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