Debaryomyces is enriched in Crohn's disease intestinal tissue and impairs healing in mice.

Debaryomyces is enriched in Crohn's disease intestinal tissue and impairs healing in mice.
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德巴利酵母菌在克罗恩病肠组织中富集,并损害小鼠的愈合。

DOI:
10.1126/science.abd0919
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发表时间:
2021-03-12
期刊:
Science (New York, N.Y.)
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与克罗恩病 (CD) 相关的菌群组成的改变很难与病理生理学的定义要素(例如损伤修复不良)联系起来。使用依赖于培养物和不依赖于培养物的方法,我们发现汉逊德巴利酵母优先定位于小鼠未完全愈合的肠道伤口和CD人类受试者发炎的粘膜组织,并且在其中大量存在。当将来自受伤小鼠和发炎 CD 组织的汉森丹氏菌培养物引入受伤的常规饲养或限生小鼠中时,会损害结肠愈合。我们从这些小鼠的受伤区域重新分离出汉逊汉森氏菌,满足科赫的假设。从机制上讲,汉森石斛通过骨髓细胞特异性 1 型干扰素 CCL5 轴损害粘膜愈合。综上所述,我们发现了一种存在于发炎的 CD 组织中并可导致粘膜愈合失调的真菌。
Alterations of the mycobiota composition associated with Crohn’s disease (CD) are challenging to link to defining elements of pathophysiology, such as poor injury repair. Using culture-dependent and -independent methods, we discovered that Debaryomyces hansenii preferentially localized to and was abundant within incompletely healed intestinal wounds of mice and inflamed mucosal tissues of CD human subjects. D. hansenii cultures from injured mice and inflamed CD tissues impaired colonic healing when introduced into injured conventionally raised or gnotobiotic mice. We reisolated D. hansenii from injured areas of these mice, fulfilling Koch’s postulates. Mechanistically, D. hansenii impaired mucosal healing through the myeloid cell–specific type 1 interferon–CCL5 axis. Taken together, we have identified a fungus that inhabits inflamed CD tissue and can lead to dysregulated mucosal healing.
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