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Abstract
BackgroundGut-derived bacterial endotoxin is an important cofactor in the pathogenesis of IBD. Regulatory T cells (Tregs) are essential for maintenance of peripheral tolerance and can prevent and alleviate IBD. To determine the immune modulatory effect of anti-LPS enriched hyperimmune colostrum, its ability to induce Tregs and alleviate immune mediated colitis.MethodsImmune-mediated colitis was induced in mice by intra-colonic instillation of Trinitrobenzene Sulfonate (TNBS). Four groups of mice were orally administered with two dosages of IgG-enriched colostrum fractions. The fractions were harvested from cows immunized against LPS derived from intestinal Escherichia coli bacteria (Imm124E). Control mice received non-immunized colostrum or vehicle (PBS). Treatment was administered one day following sensitization and four additional days following the administration of TNBS. The following parameters in the mice were tracked: body weight, bowel histology, serum cytokine levels and regulatory T cells.ResultsOral administration of Imm124E hyperimmune colostrum ameliorated immune-mediated colitis. Significant amelioration of weight reduction was noted in treated mice. Oral administration of Imm124E improved bowel histology. Both the extent of the disease, inflammation score, and colitis damage and regeneration scores decreased in Imm-124E treated animals. These effects were associated with an increase in serum IL10 anti inflammatory cytokine levels, and an increase in CD4 + CD25+ and CD4 + Foxp3+ Tregs.ConclusionsOral administration of Imm124E promoted Tregs and alleviated bowel inflammation in immune mediated colitis. The present data suggests that the microbiome may serve as a target for Tregs-based immunotherapy.Electronic supplementary materialThe online version of this article (doi:10.1186/s12876-015-0388-x) contains supplementary material, which is available to authorized users.
Highlights
Gut-derived bacterial endotoxin is an important cofactor in the pathogenesis of inflammatory bowel diseases (IBD)
Endogenous gut-derived bacterial endotoxin has been considered an important cofactor that mediates the pathogenesis of IBD [2]
Our results indicate that oral administration of Imm124E promoted regulatory T cells (Tregs) and alleviated the inflammatory state in this model
Summary
Gut-derived bacterial endotoxin is an important cofactor in the pathogenesis of IBD. Chronic inflammation involves endotoxins derived from the gut flora. Endogenous gut-derived bacterial endotoxin has been considered an important cofactor that mediates the pathogenesis of IBD [2]. Aberrant immune responses toward commensal gut bacteria result in the onset and perpetuation of IBD [3]. Antibiotics can decrease tissue invasion and eliminate aggressive bacterial species [2]. They are used in IBD to treat infective complications and for altering bacterial flora, which may result in specific anti-inflammatory effects. Therapeutic manipulation of the intestinal flora offers considerable promise for treating IBD [2]
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