1. Salmonella effector driven invasion of the gut epithelium: breaking in and setting the house on fire
- Author
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Wolf-Dietrich Hardt, Mikael E. Sellin, and Stefan A. Fattinger
- Subjects
Salmonella typhimurium ,Microbiology (medical) ,Salmonella ,Cell- och molekylärbiologi ,Inflammation ,Biology ,medicine.disease_cause ,Microbiology ,Epithelium ,Microbiology in the medical area ,Mice ,03 medical and health sciences ,Tissue culture ,Bacterial Proteins ,In vivo ,Type III Secretion Systems ,medicine ,Mikrobiologi inom det medicinska området ,Animals ,030304 developmental biology ,0303 health sciences ,030306 microbiology ,Effector ,Pathogen-associated molecular pattern ,Epithelial Cells ,Inflammasome ,3. Good health ,Gut Epithelium ,Cell biology ,Infectious Diseases ,medicine.symptom ,Cell and Molecular Biology ,medicine.drug - Abstract
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). ISSN:1369-5274 ISSN:1879-0364
- Published
- 2021