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A Novel Synthetic Mycolic Acid Inhibits Bronchial Hyperresponsiveness and Allergic Inflammation in a Mouse Model of Asthma

机译:新型合成霉菌酸抑制哮喘小鼠模型中的支气管高反应性和过敏性炎症。

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Purpose Recognition of microbes is important to trigger the innate immune system. Mycolic acid (MA) is a component of the cell walls of mycobacteria such as Mycobacterium bovis Bacillus Calmette-Guerin. MA has immunogenic properties, which may modulate the innate and adaptive immune response. This study aimed to investigate whether a novel synthetic MA (sMA) inhibits allergic inflammatory responses in a mouse model of asthma. Methods BALB/c mice were injected intraperitoneally with sMA followed by sensitization and challenge with ovalbumin (OVA). Mice were examined for bronchial hyperresponsiveness (BHR), the influx of inflammatory cells into the lung tissues, histopathological changes in the lungs and CD4+CD25+Foxp3+ T cells in the spleen, and examined the response after the depleting regulatory T cells (Tregs) with an anti-CD25mAb. Results Treatment of mice with sMA suppressed the asthmatic response, including BHR, bronchoalveolar inflammation, and pulmonary eosinophilic inflammation. Anti-CD25mAb treatment abrogated the suppressive effects of sMA in this mouse model of asthma and totally depleted CD4+CD25+Foxp3+ T cells in the spleen. Conclusions sMA attenuated allergic inflammation in a mouse model of asthma, which might be related with CD4+CD25+Foxp3+ T cell.
机译:目的识别微生物对于触发先天免疫系统很重要。分枝酸(MA)是分枝杆菌细胞壁的一种成分,例如牛分枝杆菌芽孢杆菌Calmette-Guerin。 MA具有免疫原性,可以调节先天性和适应性免疫应答。这项研究旨在调查一种新型的合成MA(sMA)是否抑制哮喘小鼠模型的过敏性炎症反应。方法对BALB / c小鼠腹腔注射sMA,然后用卵清蛋白(OVA)致敏和攻击。检查小鼠的支气管高反应性(BHR),炎性细胞流入肺组织,肺的组织病理学变化以及CD4 + CD25 + Foxp3 + <脾脏中的T细胞,并用抗CD25mAb检查耗尽调节性T细胞(Tregs)后的反应。结果sMA小鼠治疗抑制了哮喘反应,包括BHR,支气管肺泡炎症和肺嗜酸性粒细胞炎症。抗CD25mAb治疗消除了sMA在哮喘小鼠模型中的抑制作用,并且完全耗尽了CD4 + CD25 + Foxp3 + T细胞脾。结论sMA可减轻哮喘小鼠的变态反应性炎症,可能与CD4 + CD25 + Foxp3 + T细胞有关。

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