抗生素可能恶化哮喘症状
新华社 · 2014/01/19
尽管抗生素在治疗人体疾病方面是一个号帮手,然而凡事有利有弊,一项新研究证明抗生素可能会使哮喘的症状恶化。

日前,日本筑波大学的研究人员发现,服用抗生素会破坏实验鼠肠道的菌群平衡,从而使哮喘症状恶化。相关论文在线刊登在了近期的《细胞-宿主与微生物》(Cell Host & Microbe)杂志上。


研究中,科学家让实验鼠吸入会导致过敏的物质,使其患上哮喘。结果显示,如果实验鼠预先服用了抗生素,其哮喘症状比未服用抗生素的实验鼠更严重,支气管内引发炎症的细胞数量相当于后者的约 2 倍。

研究人员发现,在服用了抗生素的实验鼠肠道内,一种有害的念珠菌数量增加,它们制造的物质会激活免疫细胞,引发支气管炎症等过敏反应。使用遏制念珠菌增殖和发挥致病作用的药物后,实验鼠的哮喘症状减轻了。

该成果可能促进开发出治疗哮喘的新药。

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  • Gut Dysbiosis Promotes M2 Macrophage Polarization and Allergic Airway Inflammation via Fungi-Induced PGE2

    Although imbalances in gut microbiota composition, or “dysbiosis,” are associated with many diseases, the effects of gut dysbiosis on host systemic physiology are less well characterized. We report that gut dysbiosis induced by antibiotic (Abx) treatment promotes allergic airway inflammation by shifting macrophage polarization in the lung toward the alternatively activated M2 phenotype. Adoptive transfer of alveolar macrophages derived from Abx-treated mice was sufficient to increase allergic airway inflammation. Abx treatment resulted in the overgrowth of a commensal fungal Candida species in the gut and increased plasma concentrations of prostaglandin E2 (PGE2), which induced M2 macrophage polarization in the lung. Suppression of PGE2 synthesis by the cyclooxygenase inhibitors aspirin and celecoxib suppressed M2 macrophage polarization and decreased allergic airway inflammatory cell infiltration in Abx-treated mice. Thus, Abx treatment can cause overgrowth of particular fungal species in the gut and promote M2 macrophage activation at distant sites to influence systemic responses including allergic inflammation.

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