Effects of ceftriaxone-induced intestinal dysbacteriosis on regulatory T cells validated by anaphylactic mice

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Both probiotics and pathogens in the human gut express pathogen-associated molecular patterns (PAMPs) and die with the release of endotoxin and bacterial DNA, which can stimulate our immune system and cause immune reaction. However, it's interesting and fascinating to address why the normal intestinal flora will not generate immunological rejection like the pathogen does. By investigating the changes in cells and molecules relevant to immune tolerance in mice with ceftriaxone-induced dysbacteriosis, our study discovered that both the Evenness indexes and Shannon Wiener index of intestinal flora showed a decrease in dysbacteriosis mice. Moreover, the proportion of αβ+TCR+CD3+CD4CD8 cells, CD3+γδTCR+ cells and CD4+CD25+FoxP3+ cells in the Peyer's patches (PPs), mesenteric lymph nodes (MLNs) and spleen (SP) and the level of TGF-β1, IL-2, IL-4 and IL-10 in the serum also changed. Intestinal dysbacteriosis in an asthma murine model resulted in enhancement of immunologic response to the allergen ovalbumin (OVA), which was an agent that aggravates asthma symptoms. In summary, it is integral to maintain a certain amount or variety of intestinal microflora for regulatory T cells to act in averting hypersensitivity.HIGHLIGHTSIntestinal dysbacteriosis reduced the proportion and function of regulatory T cells in miceIntestinal dysbacteriosis enhances sensibility to allergen OVA in mice.Anaphylaxis is directly related to the dysfunction of regulatory T cells caused by intestinal flora dysbacteriosis.

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