A T-cell-independent (TI) pathway activated by microbiota results in the generation of low-affinity homeostatic IgA with a critical role in intestinal homeostasis. Moderate aerobic exercise (MAE) provides a beneficial impact on intestinal immunity, but the action of MAE on TI-IgA generation under senescence conditions is unknown. This study aimed to determine the effects of long-term MAE on TI-IgA production in young (3 month old) BALB/c mice exercised until adulthood (6 months) or aging (24 months). Lamina propria (LP) from the small intestine was obtained to determine B cell and plasma cell sub-populations by flow cytometry and molecular factors related to class switch recombination [Thymic Stromal Lymphopoietin (TSLP), A Proliferation-Inducing Ligand (APRIL), B Cell Activating Factor (BAFF), inducible nitric oxide synthase (iNOS), and retinal dehydrogenase (RDH)] and the synthesis of IgA [α-chain, interleukin (IL)-6, IL-21, and Growth Factor-β (TGF-β)]; and epithelial cells evaluated IgA transitosis [polymeric immunoglobulin receptor (pIgR), tumor necrosis factor-α (TNF-α), interferon-γ (IFN-γ), IL-4] by the RT-qPCR technique. The results were compared with data obtained from sedentary age-matched mice. Statistical analysis was computed with ANOVA, and p < 0.05 was considered to be a statistically significant difference. Under senescence conditions, MAE promoted the B cell and IgA+ B cells and APRIL, which may improve the intestinal response and ameliorate the inflammatory environment associated presumably with the downmodulation of pro-inflammatory mediators involved in the upmodulation of pIgR expression. Data suggested that MAE improved IgA and downmodulate the cytokine pro-inflammatory expression favoring homeostatic conditions in aging.

The intestinal epithelial barrier regulates paracellular transport, and its dysfunction is associated with inflammatory and metabolic diseases. Among dietary fibers, inulin has attracted considerable attention due to its beneficial effects on intestinal health. Inulin’s actions have been attributed to protecting the structure and function of gut barrier components against inflammatory-associated damage. This review integrates preclinical and clinical studies evaluating the impact of inulin on intestinal permeability. Evidence from in vitro and in vivo models shows that inulin regulates the expression of tight junction proteins (TJPs), Paneth cell proliferation, and antimicrobial peptides, and modulates inflammatory signaling pathways. In addition, inulin prebiotic activity, via microbiota, stimulates the production of short-chain fatty acids (SCFAs) as butyrate that reinforces the barrier function. Understanding these pathways highlights the therapeutic potential of inulin as a nutritional strategy for treating barrier dysfunction. Clinical studies in obesity, metabolic disorders and inflammatory intestinal disease have associated inulin supplementation with improvements in biomarkers of intestinal permeability. Future studies are needed to test inulin’s safety in order to prevent potential risks and hazards.

T-cell independent (TI) pathway activated by microbiota results in the generation of low-affinity homeostatic IgA with a critical role in intestinal homeostasis. Moderate aerobic exercise (MAE) provides a beneficial impact on intestinal immunity but the action of MAE on TI-IgA generation under senescence conditions is unknown. This study aimed to determine the effects of long-term MAE on TI-IgA production in young (3 months old) BALB/c mice exercised until adulthood (6 months) or aging (24 months). Lamina propria (LP) from the small intestine was obtained to determine B cells and plasma cells sub-populations by flow cytometry and molecular factors related to class switch recombination (TSLP/APRIL/BAFF/iNOS/RDH) and synthesis of IgA (α-chain/IL-6/IL-21/TGF-β); and epithelial cells to evaluate IgA-transitosis (pIgR/TNFα/IFN-/IL-4), by RT-qPCR technique. Results were compared with data obtained from sedentary age-matched mice. Statistical analysis was computed with ANDOVA and P<0.05 was considered as statistically significant difference. Under senescence conditions MAE promoted the B cell and IgA+B cells and APRIL that may im-prove the intestinal response and ameliorated the inflammatory environment associated pre-sumably with the downmodulation of pIgR. Data suggested that MAE improved the IgA and downmodulate the cytokine pro-inflammatory expression favoring homeostatic conditions in aging.