Author: Selinger, Christian; Tisoncik-Go, Jennifer; Menachery, Vineet D; Agnihothram, Sudhakar; Law, G Lynn; Chang, Jean; Kelly, Sara M; Sova, Pavel; Baric, Ralph S; Katze, Michael G
Title: Cytokine systems approach demonstrates differences in innate and pro-inflammatory host responses between genetically distinct MERS-CoV isolates Document date: 2014_12_22
ID: 0y3m47lh_14
Snippet: STAT3 acts as a critical regulator of cellular repair processes upon acute lung injury and BCL3 has been shown to reduce lung inflammation in mice by regulating granulocytes [27] . In addition to BCL3, several other contrasting STAT3 target genes, including BCL6, IL11, and PML, have been reported to impact pro-inflammatory responses [28] [29] [30] , epithelial integrity and the severity of lung injury after infection [27, 31] . We postulate the d.....
Document: STAT3 acts as a critical regulator of cellular repair processes upon acute lung injury and BCL3 has been shown to reduce lung inflammation in mice by regulating granulocytes [27] . In addition to BCL3, several other contrasting STAT3 target genes, including BCL6, IL11, and PML, have been reported to impact pro-inflammatory responses [28] [29] [30] , epithelial integrity and the severity of lung injury after infection [27, 31] . We postulate the difference in pro-inflammatory cytokine gene expression may be the result of differential STAT3 activity. For example, SARS-CoV directly impacts STAT3 activity by dephosphorylating STAT3 at Tyr-705 after 18 hpi in infected Vero E6 cells [32] . Here, the MERS-CoV strain-specific differences may be a causative factor in leading to differential STAT3 activation and the down-stream effects of pro-inflammatory responses.
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