The Shigella effectors prevent cell death crosstalk (IMAGE)
Caption
Host cells recognize blockade of caspase-8 apoptosis signaling by bacterial pathogens, and triggers necroptosis as a backup form of host defense. To counteract this cell death crosstalk, Shigella flexneri delivers effectors via the type III secretion system and successfully prevent apoptosis and necroptosis, thereby maintaining its replicative niche. (i) When Shigella invades and multiplies within epithelial cells, PAMPS and DAMPs are released. Host cells detect these PAMPs and DAMPs, and subsequently trigger apoptosis as host defense to clear bacterial infection. (ii) To counteract this, Shigella delivers OspC1 effector, and directly or indirectly prevents caspase-8 activation and apoptotic cell death. (iii) On the contrary, host cells detect bacterial disturbance of caspase-8 activation, resulting in induction of necroptosis as a backup host defense. (iv) Again, Shigella subsequently delivers OspD3 effector, which targets RIPK1 and RIPK3 for degradation via its protease activity to prevent necroptosis.
Credit
Department of Bacterial Pathogenesis,TMDU
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