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Abstract
The bacterium Flavonifractor plautii (FP), which is found in human feces, has been reported to participate in catechin metabolism in the gut, but this bacterium's effects on immune function are unclear. We assessed the effect of oral administration of FP on the immune response in ovalbumin (OVA) -sensitized mice. We demonstrated that the FP treatment suppressed interleukin (IL)-4 in splenocytes and OVA-specific IgE production in serum from OVA-sensitized mice. Moreover, oral administration of FP augmented CD4+CD25+ T cells and CD103+CD11c+ DCs. In animals of the FP group, the proportion of FP was increased in the mesenteric lymph nodes (MLNs), as was the proportion of Deferribacteres in the cecum. Oral administration of FP may inhibit the Th2 immune response by incorporation into the MLNs and/or by inducing changes in the gut microbiota. Thus, FP may be useful in alleviating antigen-induced Th2 immune responses.
Highlights
In recent years, the number of individuals suffering from allergic diseases has been rising globally, which has developed into an increasingly serious issue for societies worldwide [1, 2]
We found that Flavonifractor plautii (FP) decreased the numbers of IL-4+CD4+, IFN-γ+CD4+ cells (Figures 2B,C) and increased CD4+CD25+ T cells, CD103+CD11c+ dendritic cells (DCs) in spleen (Figures 2D,E)
Li et al reported that Clostridium leptum induces proliferation of Treg cells [32]; Rossi et al reported that Faecalibacterium prausnitzii strongly induces IL-10 production [33]; and Wu et al reported that decreases in the proportion of the Ruminococcaceae family induce IgE-associated eczema in infants [34]
Summary
The number of individuals suffering from allergic diseases has been rising globally, which has developed into an increasingly serious issue for societies worldwide [1, 2]. Allergic diseases are thought to be caused by a combination of genetic, lifestyle-related, and environmental factors. Both the activation of T-helper-2 (Th2) cell immune responses and the immune regulation of regulatory T cells (Tregs) have been implicated in the pathogenesis of allergic reactions [3,4,5]. Th2 cells are thought to play a key role in the onset of allergic reactions, given that this class of cells produces the pro-inflammatory cytokines interleukin (IL)-4, IL-5, and IL-13, and induces the differentiation of B cells into plasma cells. In response to stimulation by these cytokines, IL-4, B cells undergo a class switch and differentiate into plasma cells, producing high-affinity IgE antibodies [7]
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