tetano
Editor, Senior Moderator
Mediators Inflamm. 2018 Nov 8;2018:6808934. doi: 10.1155/2018/6808934. eCollection 2018.
[h=1]RIG-I Signaling via MAVS Is Dispensable for Survival in Lethal Influenza Infection In Vivo.[/h] Wu W[SUP]1[/SUP], Wang X[SUP]2[/SUP], Zhang W[SUP]1[/SUP], Tian L[SUP]1[/SUP], Booth JL[SUP]1[/SUP], Duggan ES[SUP]1[/SUP], More S[SUP]3[/SUP], Liu L[SUP]3[/SUP], Dozmorov M[SUP]4[/SUP], Metcalf JP[SUP]1,[/SUP][SUP]5,[/SUP][SUP]6[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Retinoic acid-inducible gene I (RIG-I) is an important regulator of virus-induced antiviral interferons (IFNs) and proinflammatory cytokines. It requires interaction with an adaptor molecule, mitochondrial antiviral-signaling protein (MAVS), to activate downstream signaling pathways. To elucidate the mechanism(s) by which RIG-I-dependent recognition of IAV infection in vivo triggers innate immune responses, we infected mutant mice lacking RIG-I or MAVS with influenza A virus (IAV) and measured their innate immune responses. As has previously been demonstrated with isolated deletion of the virus recognition receptors TLR3, TLR7, and NOD2, RIG-I or MAVS knockout (KO) did not result in higher mortality and did not reduce IAV-induced cytokine responses in mice. Infected RIG-I KO animals displayed similar lung inflammation profiles as did WT mice, in terms of the protein concentration, total cell count, and inflammatory cell composition in the bronchoalveolar lavage fluid. RNA-Seq results demonstrated that all types of mice exhibited equivalent antiviral and inflammatory gene responses following IAV infection. Together, the results indicated that although RIG-I is important in innate cytokine responses in vitro, individual deletion of the genes encoding RIG-I or MAVS did not change survival or innate responses in vivo after IAV infection in mice.
PMID: 30532653 PMCID: PMC6250004 DOI: 10.1155/2018/6808934
Free PMC Article
[h=1]RIG-I Signaling via MAVS Is Dispensable for Survival in Lethal Influenza Infection In Vivo.[/h] Wu W[SUP]1[/SUP], Wang X[SUP]2[/SUP], Zhang W[SUP]1[/SUP], Tian L[SUP]1[/SUP], Booth JL[SUP]1[/SUP], Duggan ES[SUP]1[/SUP], More S[SUP]3[/SUP], Liu L[SUP]3[/SUP], Dozmorov M[SUP]4[/SUP], Metcalf JP[SUP]1,[/SUP][SUP]5,[/SUP][SUP]6[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Retinoic acid-inducible gene I (RIG-I) is an important regulator of virus-induced antiviral interferons (IFNs) and proinflammatory cytokines. It requires interaction with an adaptor molecule, mitochondrial antiviral-signaling protein (MAVS), to activate downstream signaling pathways. To elucidate the mechanism(s) by which RIG-I-dependent recognition of IAV infection in vivo triggers innate immune responses, we infected mutant mice lacking RIG-I or MAVS with influenza A virus (IAV) and measured their innate immune responses. As has previously been demonstrated with isolated deletion of the virus recognition receptors TLR3, TLR7, and NOD2, RIG-I or MAVS knockout (KO) did not result in higher mortality and did not reduce IAV-induced cytokine responses in mice. Infected RIG-I KO animals displayed similar lung inflammation profiles as did WT mice, in terms of the protein concentration, total cell count, and inflammatory cell composition in the bronchoalveolar lavage fluid. RNA-Seq results demonstrated that all types of mice exhibited equivalent antiviral and inflammatory gene responses following IAV infection. Together, the results indicated that although RIG-I is important in innate cytokine responses in vitro, individual deletion of the genes encoding RIG-I or MAVS did not change survival or innate responses in vivo after IAV infection in mice.
PMID: 30532653 PMCID: PMC6250004 DOI: 10.1155/2018/6808934
Free PMC Article