Abstract
The current therapy on allergic inflammation is unsatisfactory. Probiotics improve the immunity in the body. This study aims to test a hypothesis that administration with Clostridium butyricum (C. butyricum) enforces the effect of specific immunotherapy (SIT) on intestinal allergic inflammation. In this study, an ovalbumin (OVA) specific allergic inflammation mouse model was created. The mice were treated with SIT or/and C. butyricum. The results showed that the intestinal allergic inflammation was only moderately alleviated by SIT, which was significantly enforced by a combination with C. butyricum; treating with C. butyricum alone did not show much inhibitory efficacy. The increase in the frequency of the interleukin (IL)-10-producing OVA-specific B cell (OVAsBC) was observed in mice in parallel to the inhibitory effect on the intestinal allergic inflammation. The in vitro treatment of the OVAsBCs with OVA increased the histone deacetylase-1 (HDAC1) phosphorylation, modulated the transcription of the Bcl6 gene, and triggered the OVAsBCs to differentiate to the IgE-producing plasma cells. Exposure to both OVA and butyrate sodium in the culture increased the expression of IL-10 in OVAsBCs. In conclusion, administration with C. butyricum enforces the inhibitory effect of SIT on allergic inflammation in the mouse intestine.
Highlights
Further develop into plasma cells with the capacity to produce antigen specific IgE
The results showed that Specific immunotherapy (SIT) moderately improved the allergic inflammation in the intestine, which was markedly enforced by the addition of C. butyricum; while treatment with C. butyricum alone did not apparently inhibit the intestinal inflammation (Fig. 1)
The results showed that the frequency of TGF-β positive cells was only slightly increased (Fig. 2A–D) while the treatment with SIT/C. butyricum markedly increased the frequency of IL-10 positive cells in lamina propria mononuclear cells (LPMC), which did not occur in mice treated with either SIT alone or C. butyricum alone (Fig. 2E–H)
Summary
Further develop into plasma cells with the capacity to produce antigen specific IgE. Upon re-exposure to specific antigens, the Tregs and Bregs are activated to release immune suppressor mediators, such as IL-10 and transforming growth factor-β , to suppress other effector T cell activities, to inhibit the allergic inflammation[8]. Probiotics may inhibit inflammation and/or activate innate immunity in the intestine, which can be used within therapeutic strategies to restore the host gut microbiota[11]. Probiotics contribute to the maintenance of the intestinal homeostasis via activating Toll like receptor 412. It seems that probiotics benefit the host immunity; yet, the underlying mechanism remains to be further elucidated. The results showed that administration of C. butyricum markedly enforced the therapy of SIT on the antigen specific allergic inflammation in the intestine. The C. butyricum-derived butyrate regulated the signal transduction pathway of IgE production in antigen specific B cells and induced IL-10 expression
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