Department of Pediatric Gastroenterology and Nutrition, Harvard Medical School and Massachusetts General Hospital, Boston, MA 02129, USA.
Department of Molecular Genetics and Microbiology, University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, MA 01655, USA.
Science. 2010 Oct 15;330(6002):390-393. doi: 10.1126/science.1194598.
The enteric pathogen Salmonella enterica serovar Typhimurium causes food poisoning resulting in gastroenteritis. The S. Typhimurium effector Salmonella invasion protein A (SipA) promotes gastroenteritis by functional motifs that trigger either mechanisms of inflammation or bacterial entry. During infection of intestinal epithelial cells, SipA was found to be responsible for the early activation of caspase-3, an enzyme that is required for SipA cleavage at a specific recognition motif that divided the protein into its two functional domains and activated SipA in a manner necessary for pathogenicity. Other caspase-3 cleavage sites identified in S. Typhimurium appeared to be restricted to secreted effector proteins, which indicates that this may be a general strategy used by this pathogen for processing of its secreted effectors.
肠病原体沙门氏菌肠炎血清型引起食物中毒导致肠胃炎。沙门氏菌肠炎侵袭蛋白 A（SipA）通过触发炎症机制或细菌进入的功能基序促进肠胃炎。在肠上皮细胞感染期间，发现 SipA 负责 caspase-3 的早期激活，caspase-3 是一种酶，需要在特定识别基序处切割 SipA，该基序将蛋白质分为两个功能域，并以对致病性必需的方式激活 SipA。在肠炎沙门氏菌中鉴定的其他 caspase-3 切割位点似乎仅限于分泌效应蛋白，这表明这可能是该病原体用于处理其分泌效应蛋白的一般策略。
