澳大利亚莫纳什大学Benjamin J. Marsland等研究人员合作发现，早期抗生素导致的菌群失调会破坏吲哚-3-丙酸的产生，并加剧成年后的过敏性气道炎症。相关论文于2024年7月15日在线发表在《免疫》杂志上。

研究人员发现，早期使用抗生素（EL-Abx）的鼠类，而不是成年期使用抗生素的鼠类，更容易受到屋尘螨（HDM）诱导的过敏性气道炎症的影响。这种易感性在肠道微生物群恢复正常后仍然存在。EL-Abx降低了系统性吲哚-3-丙酸（IPA）的水平，IPA在肺上皮细胞中诱导了对细胞应激、代谢和线粒体呼吸的长期改变。

IPA减少了线粒体呼吸和超氧化物的生成，并改变了趋化因子和细胞因子的生成。因此，早期补充IPA可以保护EL-Abx鼠类免受成年期HDM诱导的加重的过敏性气道炎症。该研究揭示了EL-Abx如何使肺部易感过敏性气道炎症的机制，并提出了一种可能的预防方法，以减轻EL-Abx的有害后果。

据介绍，早期使用抗生素会破坏微生物的定殖，并增加过敏和哮喘的发病风险。

附：英文原文

Title: Antibiotic-driven dysbiosis in early life disrupts indole-3-propionic acid production and exacerbates allergic airway inflammation in adulthood

Author: Olaf Perdijk, Alana Butler, Matthew Macowan, Roxanne Chatzis, Edyta Bulanda, Rhiannon D. Grant, Nicola L. Harris, Tomasz P. Wypych, Benjamin J. Marsland

Issue&Volume: 2024-07-15

Abstract: Antibiotic use in early life disrupts microbial colonization and increases the riskof developing allergies and asthma. We report that mice given antibiotics in earlylife (EL-Abx), but not in adulthood, were more susceptible to house dust mite (HDM)-inducedallergic airway inflammation. This susceptibility was maintained even after normalizationof the gut microbiome. EL-Abx decreased systemic levels of indole-3-propionic acid(IPA), which induced long-term changes to cellular stress, metabolism, and mitochondrialrespiration in the lung epithelium. IPA reduced mitochondrial respiration and superoxideproduction and altered chemokine and cytokine production. Consequently, early-lifeIPA supplementation protected EL-Abx mice against exacerbated HDM-induced allergicairway inflammation in adulthood. These results reveal a mechanism through which EL-Abxcan predispose the lung to allergic airway inflammation and highlight a possible preventativeapproach to mitigate the detrimental consequences of EL-Abx.

DOI: 10.1016/j.immuni.2024.06.010

Source: https://www.cell.com/immunity/abstract/S1074-7613(24)00316-9