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肠道共生真菌Wallemia mellicola 通过 Dectin-2 增强小鼠哮喘。

The intestinal commensal fungus Wallemia mellicola enhances asthma in mice through Dectin-2.

机构信息

Division of Pulmonary and Critical Care Medicine, Mayo Clinic, Rochester, MN USA.

Thoracic Disease Research Unit, Department of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, MN USA.

出版信息

Med Mycol. 2024 Jan 27;62(2). doi: 10.1093/mmy/myae004.

Abstract

Overgrowth of the fungus Wallemia mellicola in the intestines of mice enhances the severity of asthma. Wallemia mellicola interacts with the immune system through Dectin-2 expressed on the surface of myeloid and intestinal epithelial cells. Using Dectin-2-deficient mice, we show that the interaction of W. mellicola with Dectin-2 is essential for the gut-lung pathways, enhancing the severity of asthma in mice with W. mellicola intestinal dysbiosis. These findings offer better insight into dysbiosis-associated inflammation and highlight the role pattern recognition receptors have in immune recognition of commensal fungi in the gut, leading to alterations in immune function in the lungs.

摘要

黑曲霉在肠道中的过度生长会加重哮喘的严重程度。黑曲霉通过表达在髓样细胞和肠道上皮细胞表面的 Dectin-2 与免疫系统相互作用。利用 Dectin-2 缺陷型小鼠,我们发现黑曲霉与 Dectin-2 的相互作用对于肠道-肺部途径是必需的,可增强黑曲霉肠道菌群失调小鼠哮喘的严重程度。这些发现为与菌群失调相关的炎症提供了更好的认识,并强调了模式识别受体在肠道共生真菌免疫识别中的作用,导致肺部免疫功能的改变。

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