tetano
Editor, Senior Moderator
EMBO J. 2018 Oct 15. pii: e99176. doi: 10.15252/embj.201899176. [Epub ahead of print]
[h=1]Loss of T-bet confers survival advantage to influenza-bacterial superinfection.[/h] Er JZ[SUP]1[/SUP], Koean RAG[SUP]2[/SUP], Ding JL[SUP]3,[/SUP][SUP]2[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] The transcription factor, T-bet, regulates type 1 inflammatory responses against a range of infections. Here, we demonstrate a previously unaddressed role of T-bet, to influenza virus and bacterial superinfection. Interestingly, we found that T-bet deficiency did not adversely affect the efficacy of viral clearance or recovery compared to wild-type hosts. Instead, increased infiltration of neutrophils and production of Th17 cytokines (IL-17 and IL-22), in lungs of influenza virus-infected T-bet[SUP]-/-[/SUP] mice, were correlated with survival advantage against subsequent infection by Streptococcus pneumoniae Neutralization of IL-17, but not IL-22, in T-bet[SUP]-/-[/SUP] mice increased pulmonary bacterial load, concomitant with decreased neutrophil infiltration and reduced survival of T-bet[SUP]-/-[/SUP] mice. IL-17 production by CD8[SUP]+[/SUP], CD4[SUP]+[/SUP] and γδ T cell types was identified to contribute to this protection against bacterial superinfection. We further showed that neutrophil depletion in T-bet[SUP]-/-[/SUP] lungs increased pulmonary bacterial burden. These results thus indicate that despite the loss of T-bet, immune defences required for influenza viral clearance are fully functional, which in turn enhances protective type 17 immune responses against lethal bacterial superinfections.
[h=4]KEYWORDS:[/h] Streptococcus pneumonia ; T‐bet; bacteria; influenza
PMID: 30322895 DOI: 10.15252/embj.201899176
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[h=1]Loss of T-bet confers survival advantage to influenza-bacterial superinfection.[/h] Er JZ[SUP]1[/SUP], Koean RAG[SUP]2[/SUP], Ding JL[SUP]3,[/SUP][SUP]2[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] The transcription factor, T-bet, regulates type 1 inflammatory responses against a range of infections. Here, we demonstrate a previously unaddressed role of T-bet, to influenza virus and bacterial superinfection. Interestingly, we found that T-bet deficiency did not adversely affect the efficacy of viral clearance or recovery compared to wild-type hosts. Instead, increased infiltration of neutrophils and production of Th17 cytokines (IL-17 and IL-22), in lungs of influenza virus-infected T-bet[SUP]-/-[/SUP] mice, were correlated with survival advantage against subsequent infection by Streptococcus pneumoniae Neutralization of IL-17, but not IL-22, in T-bet[SUP]-/-[/SUP] mice increased pulmonary bacterial load, concomitant with decreased neutrophil infiltration and reduced survival of T-bet[SUP]-/-[/SUP] mice. IL-17 production by CD8[SUP]+[/SUP], CD4[SUP]+[/SUP] and γδ T cell types was identified to contribute to this protection against bacterial superinfection. We further showed that neutrophil depletion in T-bet[SUP]-/-[/SUP] lungs increased pulmonary bacterial burden. These results thus indicate that despite the loss of T-bet, immune defences required for influenza viral clearance are fully functional, which in turn enhances protective type 17 immune responses against lethal bacterial superinfections.
[h=4]KEYWORDS:[/h] Streptococcus pneumonia ; T‐bet; bacteria; influenza
PMID: 30322895 DOI: 10.15252/embj.201899176
Free full text