Rickettsia species of the spotted fever group are arthropod-borne obligate intracellular bacteria that can cause mild to severe human disease. These bacteria invade host cells, replicate in the cell cytosol, and spread from cell to cell. To access the host cytosol and avoid immune detection, they escape membrane-bound vacuoles by expressing factors that disrupt host membranes. Here, we show that a patatin-like phospholipase A2 enzyme (Pat1) facilitates Rickettsia parkeri infection by promoting escape from host membranes and cell-cell spread. Pat1 is important for infection in a mouse model and, at the cellular level, is crucial for efficiently escaping from single and double membrane-bound vacuoles into the host cytosol, and for avoiding host galectins that mark damaged membranes. Pat1 is also important for avoiding host polyubiquitin, preventing recruitment of autophagy receptor p62, and promoting actin-based motility and cell-cell spread.

斑疹热组的立克次体是节肢动物传播的专性细胞内细菌，可导致轻度至重度人类疾病。这些细菌侵入宿主细胞，在细胞质中复制，并在细胞间传播。为了接近宿主细胞质并避免免疫检测，它们通过表达破坏宿主细胞膜的因子来逃离膜结合液泡。在这里，我们展示了一种类似patatin 的磷脂酶A2 酶（Pat1）促进立克次氏体通过促进从宿主细胞膜逃逸和细胞间扩散来感染。Pat1 对于小鼠模型中的感染很重要，并且在细胞水平上，对于有效地从单膜结合液泡和双膜结合液泡逃逸到宿主胞质溶胶中以及避免标记受损膜的宿主半乳凝素至关重要。Pat1 对于避免宿主多泛素、防止自噬受体 p62 的募集以及促进基于肌动蛋白的运动和细胞间扩散也很重要。