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Viral infection augments Nod1/2 signaling to potentiate lethality associated with secondary bacterial infections.

Authors: Kim, YG  Park, JH  Reimer, T  Baker, DP  Kawai, T  Kumar, H  Akira, S  Wobus, C  Nunez, G 
Citation: Kim YG, etal., Cell Host Microbe. 2011 Jun 16;9(6):496-507.
Pubmed: (View Article at PubMed) PMID:21669398
DOI: Full-text: DOI:10.1016/j.chom.2011.05.006

Secondary bacterial infection is a common sequela to viral infection and is associated with increased lethality and morbidity. However, the underlying mechanisms remain poorly understood. We show that the TLR3/MDA5 agonist poly I:C or viral infection dramatically augments signaling via the NLRs Nod1 and Nod2 and enhances the production of proinflammatory cytokines. Enhanced Nod1 and Nod2 signaling by poly I:C required the TLR3/MDA5 adaptors TRIF and IPS-1 and was mediated by type I IFNs. Mechanistically, poly I:C or IFN-beta induced the expression of Nod1, Nod2, and the Nod-signaling adaptor Rip2. Systemic administration of poly I:C or IFN-beta or infection with murine norovirus-1 promoted inflammation and lethality in mice superinfected with E. coli, which was independent of bacterial burden but attenuated in the absence of Nod1/Nod2 or Rip2. Thus, crosstalk between type I IFNs and Nod1/Nod2 signaling promotes bacterial recognition, but induces harmful effects in the virally infected host.

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RGD Object Information
RGD ID: 5508748
Created: 2011-10-20
Species: All species
Last Modified: 2011-10-20
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.