Salmonella Typhimurium (S.Tm) is a major cause of diarrheal disease. The invasion into intestinal epithelial cells (IECs) is a central step in the infection cycle. It is associated with gut inflammation and thought to benefit S.Tm proliferation also in the intestinal lumen. Importantly, it is still not entirely clear how inflammation is elicited and to which extent it links to IEC invasion efficiency in vivo. In this review, we summarize recent findings explaining IEC invasion by type-three-secretion-system-1 (TTSS-1) effector proteins and discuss their effects on invasion and gut inflammation. In non-polarized tissue culture cells, the TTSS-1 effectors (mainly SopB/E/E2) elicit large membrane ruffles fueling cooperative invasion, and can directly trigger pro-inflammatory signaling. By contrast, in the murine gut, we observe discreet-invasion (mainly via the TTSS-1 effector SipA) and a prominent pro-inflammatory role of the host?"s epithelial inflammasome(s), which sense pathogen associated molecular patterns (PAMPs). We discuss why it has remained a major challenge to tease apart direct and indirect inflammatory effects of TTSS-1 effectors and explain why further research will be needed to fully determine their inflammation-modulating role(s).

沙门氏菌鼠伤寒沙门氏菌（小号.Tm）是腹泻病的主要病因。侵入肠上皮细胞 (IEC) 是感染周期的核心步骤。它与肠道炎症有关，并认为受益小号肠腔也.Tm增殖。重要的是，仍然不完全清楚炎症是如何引发的，以及它在多大程度上与体内IEC 侵袭效率有关. 在这篇综述中，我们总结了解释 1 型三分泌系统 (TTSS-1) 效应蛋白对 IEC 侵袭的最新发现，并讨论了它们对侵袭和肠道炎症的影响。在非极化的组织培养细胞中，TTSS-1 效应子（主要是 SopB/E/E2）引发大的膜褶皱，促进协同入侵，并可以直接触发促炎信号。相比之下，在小鼠肠道中，我们观察到谨慎的入侵（主要通过 TTSS-1 效应子 SipA）和宿主的显着促炎作用？我们讨论了为什么区分 TTSS-1 效应子的直接和间接炎症作用仍然是一个主要挑战，并解释为什么需要进一步研究来充分确定它们的炎症调节作用。