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Fig. 2 | Virology Journal

Fig. 2

From: Oxidative stress and ROS-mediated cellular events in RSV infection: potential protective roles of antioxidants

Fig. 2

ROS-mediated NLRP3 inflammasome activation and lytic cell death in RSV-infected macrophages. Signal 1: Activation of the TLR/Myd88/NF-κB pathway promotes the expression of NLRP3,pro-IL-1β, and pro-IL-18. Signal 2: RSV-induced ROS overproduction and potassium (K+) efflux as well as mitochondrial dysfunction contribute to NLRP3 inflammasome activation, leading to caspase 1 activation, which induces the cleavage of pro-IL-1β and pro-IL-18 into their mature and biologically active forms. Lytic cell death mechanisms: ASC-NLRP3 inflammasome-dependent caspase-1 activation promotes pyroptotic cell death and may also partially contribute to activation of the necroptosis pathway in RSV-infected macrophages during RSV infection. The RIPK3/MLKL pathway plays a positive regulatory role in necroptosis. The pivotal role of ROS in promoting lytic cell death in RSV-infected macrophages is also highlighted

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Virology Journal

ISSN: 1743-422X