The role of the tumor suppressor CYLD in Yersinia enterocolitica infection

摘要: Recent studies have identified the tumor suppressor CYLD as a key regulator of NF -κB, transcription factor that promotes cell survival and oncogenesis, well host defence to infection. In th e pr esent study, we investigated role in regulation innate immune responses mice Y. enterocolitica infection for comparison Salmonella Typhimurium . Yersinia is an extracellular multiplying bacterium ensures its growth by injecting virulence proteins (Yops) into cells injectisome Ysc-T3SS , which interfere with several signaling pathways (such MAPK NF-κB cascades), resulting in inhibition phagocytosis, oxidative burst cytokine production. contrast, endowed 2 T3SS inject effector induce pathogen uptake intracellular replication. Surprisingly, found Cyld-/- were more resistant than Cyld+/- mice contrast Typimurium appeared be CYLD- independent. These results suggest acts detrimental during early infection. Furthermore, showed Yops-mediated defense mechanisms such burst, NF-κB, production p38 activation attenuated Cyld-/--phagocytic respect Cyld+/- cells. Taken together, this study provides first time, empirical demonstration a pathogen-specific contribution gene encoded protein, respectively, CYLD, susceptibility manner seems independent suppression mechanism. This another example extraordinary complexity pathogen/host interactions.