Different effector arms of the immune system are optimized to protect from different classes of pathogens. In some cases, pathogens manipulate the host immune system to promote 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 as an energy source by the pathogen. Specifically, P. aeruginosa-secreted toxin, LasB, processed and activated epithelial amphiregulin to induce type 2 inflammation and mucin production. This “niche remodeling” by P. aeruginosa promoted colonization and, as a by-product, allergic sensitization. Our study thus reveals a type of bacterial immune deviation by increasing nutrient supply. It also uncovers a mechanism of allergic sensitization by a bacterial virulence factor.

免疫系统的不同效应臂经过优化，可抵御不同类别的病原体。在某些情况下，病原体会操纵宿主免疫系统，促进错误类型的效应反应，这种现象称为免疫偏差。通常，免疫偏差有助于病原体避免破坏性的免疫反应。在这里，我们报告了一种免疫偏差，其中机会性病原体铜绿假单胞菌( P. aeruginosa ) 诱导 2 型免疫反应，导致粘蛋白产生，粘蛋白被病原体用作能量来源。具体来说， P .铜绿假单胞菌分泌的毒素 LasB 加工并激活上皮双调蛋白，诱导 2 型炎症和粘蛋白产生。 P的这种“利基重塑”。铜绿假单胞菌促进定植，并作为副产品促进过敏性致敏。因此，我们的研究揭示了一种通过增加营养供应而导致的细菌免疫偏差。它还揭示了细菌毒力因子引起过敏的机制。