美国耶鲁大学Ruslan Medzhitov研究组发现，机会型病原体的组织重塑引发过敏性炎症。相关论文于2022年4月27日在线发表在《免疫》杂志上。

研究人员报告了一种免疫偏离，即机会型病原体铜绿假单胞菌（P. aeruginosa）诱导2型免疫反应，导致粘液蛋白的产生，被病原体用作能量来源。具体来说，P. aeruginosa分泌的毒素LasB加工并激活上皮细胞的双调蛋白，从而诱导2型炎症和粘液蛋白的产生。P. aeruginosa的这种"微环境重塑"促进了定植，并作为一种副产品促进了过敏性过敏。因此，这项研究揭示了一种通过增加营养供应的细菌免疫偏离。它还发现了一种由细菌毒力因子引起的过敏性敏感的机制。

据悉，免疫系统的不同效应臂被优化以保护免受不同类别病原体的侵害。在某些情况下，病原体操纵宿主的免疫系统以促进错误类型的效应器反应，这种现象被称为免疫偏离。通常情况下，免疫偏离帮助病原体避免破坏性的免疫反应。

附：英文原文

Title: Tissue remodeling by an opportunistic pathogen triggers allergic inflammation

Author: Karen Agaronyan, Lokesh Sharma, Bharat Vaidyanathan, Keith Glenn, Shuang Yu, Charles Annicelli, Talia D. Wiggen, Mitchell R. Penningroth, Ryan C. Hunter, Charles S. Dela Cruz, Ruslan Medzhitov

Issue&Volume: 2022-04-27

Abstract: Different effector arms of the immune system are optimized to protect from differentclasses of pathogens. In some cases, pathogens manipulate the host immune system topromote the wrong type of effector response—a phenomenon known as immune deviation.Typically, immune deviation helps pathogens to avoid destructive immune responses.Here, we report on a type of immune deviation whereby an opportunistic pathogen, Pseudomonas aeruginosa (P. aeruginosa), induces the type 2 immune response resulting in mucin production that is used asan energy source by the pathogen. Specifically, P. aeruginosa-secreted toxin, LasB, processed and activated epithelial amphiregulin to induce type2 inflammation and mucin production. This “niche remodeling” by P. aeruginosa promoted colonization and, as a by-product, allergic sensitization. Our study thusreveals a type of bacterial immune deviation by increasing nutrient supply. It alsouncovers a mechanism of allergic sensitization by a bacterial virulence factor.

DOI: 10.1016/j.immuni.2022.04.001

Source: https://www.cell.com/immunity/fulltext/S1074-7613(22)00172-8