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Concerning Bifidobacterium longum & Ulcerative Colitis (UC), Bifidobacterium longum has shown therapeutic potential in ulcerative colitis by improving the intestinal barrier, modulating the immune system, and regulating the microbiota. Preclinical studies and clinical trials both support its use as an adjunctive or alternative treatment for UC, with effects that vary depending on the strain and host factors (1)
Bifidobacterium longum alleviates ulcerative colitis (UC) through multiple mechanisms. This bacterium enhances the function of the intestinal barrier by boosting tight junction proteins and decreasing intestinal permeability. It also has anti-inflammatory effects, as it increases IL-10 production in peripheral blood mononuclear cells and inhibits the secretion of the pro-inflammatory cytokine Chemokine (C-X-C motif) ligand 8 (CXCL8) / Interleukin-8 (IL-8) in intestinal epithelial cells. Furthermore, Bifidobacterium longum suppresses the formation of the NLRP3 inflammasome by downregulating Human GBP5 expression in macrophages and reduces inflammation by inhibiting the NFKB signaling pathway. In addition, it mitigates oxidative stress by activating the Nrf2 Signal transduction pathway (2)
The therapeutic effectiveness of Bifidobacterium longum varies significantly depending on the strain. For instance, Bifidobacterium longum longum CCM 7952 was effective in preventing DSS-induced colitis and enhancing barrier function, but this was strictly specific to the strain. In contrast, another strain, Bifidobacterium longum 372, did not exhibit any protective effects. Strains such as Bifidobacterium longum 35624 and Bifidobacterium longum 1714 have shown anti-inflammatory benefits in patients with ulcerative colitis (UC). Additionally, pretreatment with Bifidobacterium longum BAA2573 notably improved symptoms and histopathological damage by influencing pathways related to starch metabolism, vitamin B6 metabolism, and sphingolipid metabolism (2, 3)
Extracellular vesicles derived from Bifidobacterium longum NSP001 (NEVs) have been shown to improve intestinal barrier function. They also modulate T cell differentiation, promote SCFA production, and suppress the STAT3 pathway. These effects occur in both microbiota-dependent and independent manners (4)
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see also:
Barrier Permeability / Intestinal Permeability & Tight-Junction Molecules / Tight Junction Proteins
Bifidobacterium / Bifidobacter & Ulcerative colitis (UC)
Bifidobacterium longum & Inflammatory Bowel Disease (IBD)
Epithelial Barrier Integrity / Mucosal Barrier Integrity & Tight-Junction Molecules / Tight Junction Proteins
Macrophages (CD68s) & NFKB Signaling / NFKB Pathway
Probiotics (living agents) & Ulcerative Colitis (UC)
Ulcerative colitis (UC) & Drugs/Treatments