E1 ReplicatedModerate confidencePEM not requiredRCTPeer-reviewedReviewed
Standard · 3 min
Bifidobacterium infantis 35624 modulates host inflammatory processes beyond the gut.
Groeger, David, O'Mahony, Liam, Murphy, Eileen F et al. · Gut microbes · 2013 · DOI
Quick Summary
This study tested whether a beneficial gut bacterium called Bifidobacterium infantis 35624 could reduce inflammation in people with ME/CFS, along with people who have other inflammatory conditions like ulcerative colitis and psoriasis. Participants took either the bacterium or placebo for 6-8 weeks, and researchers measured inflammatory markers in their blood. The bacterium reduced multiple inflammatory markers across all three conditions, suggesting that gut bacteria can influence immune system activity throughout the whole body, not just in the gut.
Why It Matters
This study provides evidence that specific probiotics may help reduce systemic inflammation in ME/CFS—a condition where dysregulated immune and inflammatory responses are thought to play a central role. The finding that a single bacterial strain can reduce inflammatory cytokines in ME/CFS alongside other conditions suggests a plausible mechanistic pathway for microbiota-based interventions. This work supports the rationale for investigating targeted probiotic therapies as potential adjunctive treatments for ME/CFS.
Observed Findings
Plasma CRP levels were significantly reduced by B. infantis 35624 in all three inflammatory disorders (UC, CFS, psoriasis) compared to placebo.
Plasma TNF-α was reduced in CFS and psoriasis patients receiving B. infantis 35624.
Plasma IL-6 was reduced in UC and CFS patients receiving B. infantis 35624.
In healthy subjects, LPS-stimulated TNF-α and IL-6 secretion by PBMCs was significantly reduced after 8 weeks of B. infantis 35624 treatment.
Inferred Conclusions
B. infantis 35624 exerts immunoregulatory effects that reduce systemic pro-inflammatory biomarkers in both gastrointestinal and non-gastrointestinal inflammatory conditions.
The immunomodulatory effects of commensal microbiota extend beyond the mucosal immune system to influence systemic immune responses.
This probiotic strain may have therapeutic potential across multiple inflammatory disorders through shared mechanisms of immune regulation.
Remaining Questions
Do reductions in inflammatory biomarkers translate to clinically meaningful symptom improvement in ME/CFS patients?
Which mechanisms explain how B. infantis 35624 influences systemic immune function—through intestinal barrier effects, metabolite production, or other pathways?
What This Study Does Not Prove
This study does not prove that B. infantis 35624 will be clinically effective or improve ME/CFS symptoms—only that it can reduce certain inflammatory markers. The study does not establish causation between inflammation reduction and symptom improvement, nor does it identify which ME/CFS patients might benefit or determine the optimal dosing or duration of treatment. The mechanisms by which this bacterium influences systemic immunity remain unclear from this data alone.
About the PEM badge: “PEM required” means post-exertional malaise was an explicit required diagnostic criterion for participant inclusion in this study — not that PEM was studied, observed, or discussed. Studies using criteria that do not require PEM (e.g. Fukuda, Oxford) are tagged “PEM not required”. How the atlas works →
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Are there patient subgroups within ME/CFS (defined by immune profile, disease duration, or other factors) that respond preferentially to this intervention?
What is the durability of the anti-inflammatory effect after treatment cessation, and what maintenance dosing might be required?