tetano
Editor, Senior Moderator
Sci Rep. 2017 Aug 22;7(1):9128. doi: 10.1038/s41598-017-08030-w.
[h=1]Pulmonary inflammation and cytokine dynamics of bronchoalveolar lavage fluid from a mouse model of bronchial asthma during A(H1N1)pdm09 influenza infection.[/h] Fujimoto Y[SUP]1[/SUP], Hasegawa S[SUP]2[/SUP], Matsushige T[SUP]1[/SUP], Wakiguchi H[SUP]1[/SUP], Nakamura T[SUP]1[/SUP], Hasegawa H[SUP]3[/SUP], Nakajima N[SUP]3[/SUP], Ainai A[SUP]3[/SUP], Oga A[SUP]4[/SUP], Itoh H[SUP]4[/SUP], Shirabe K[SUP]5[/SUP], Toda S[SUP]5[/SUP], Atsuta R[SUP]6[/SUP], Morishima T[SUP]7[/SUP], Ohga S[SUP]1[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Asthmatic patients present more rapid progression of respiratory distress after A(H1N1)pdm09 influenza infection than after seasonal infection. Here, we sought to clarify the pathophysiology of early deterioration in asthmatic patients after A(H1N1)pdm09 infection. Cytokine levels and virus titres in bronchoalveolar lavage fluid from mice with and without asthma after A(H1N1)pdm09 or seasonal H1N1 infection were examined. In asthma/A(H1N1)pdm09 mice, IL-6 and TNF-α levels peaked at 3 days post-infection and were higher than those in all other groups. IFN-γ levels in asthma/A(H1N1)pdm09 mice at 3 days post-infection were higher than in all other mice at any time point, whereas at 7 days post-infection, the levels were lowest in asthma/A(H1N1)pdm09 mice. Virus titres in asthma/A(H1N1)pdm09 mice were highest at 3 days post-infection, and decreased by 7 days post-infection, although the levels at this time point were still higher than that in any other group. Histopathological examination showed more inflammatory cell infiltration and lung tissue destruction in the asthma/A(H1N1)pdm09 group than in any other group. The distinct cytokine profiles in A(H1N1)pdm09-infected asthmatic mice indicated excessive inflammation and virus replication within a few days after infection. Thus, bronchial asthma could be a more exacerbating factor for pandemic influenza infection than for seasonal influenza infection.
PMID: 28831046 DOI: 10.1038/s41598-017-08030-w
[h=1]Pulmonary inflammation and cytokine dynamics of bronchoalveolar lavage fluid from a mouse model of bronchial asthma during A(H1N1)pdm09 influenza infection.[/h] Fujimoto Y[SUP]1[/SUP], Hasegawa S[SUP]2[/SUP], Matsushige T[SUP]1[/SUP], Wakiguchi H[SUP]1[/SUP], Nakamura T[SUP]1[/SUP], Hasegawa H[SUP]3[/SUP], Nakajima N[SUP]3[/SUP], Ainai A[SUP]3[/SUP], Oga A[SUP]4[/SUP], Itoh H[SUP]4[/SUP], Shirabe K[SUP]5[/SUP], Toda S[SUP]5[/SUP], Atsuta R[SUP]6[/SUP], Morishima T[SUP]7[/SUP], Ohga S[SUP]1[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Asthmatic patients present more rapid progression of respiratory distress after A(H1N1)pdm09 influenza infection than after seasonal infection. Here, we sought to clarify the pathophysiology of early deterioration in asthmatic patients after A(H1N1)pdm09 infection. Cytokine levels and virus titres in bronchoalveolar lavage fluid from mice with and without asthma after A(H1N1)pdm09 or seasonal H1N1 infection were examined. In asthma/A(H1N1)pdm09 mice, IL-6 and TNF-α levels peaked at 3 days post-infection and were higher than those in all other groups. IFN-γ levels in asthma/A(H1N1)pdm09 mice at 3 days post-infection were higher than in all other mice at any time point, whereas at 7 days post-infection, the levels were lowest in asthma/A(H1N1)pdm09 mice. Virus titres in asthma/A(H1N1)pdm09 mice were highest at 3 days post-infection, and decreased by 7 days post-infection, although the levels at this time point were still higher than that in any other group. Histopathological examination showed more inflammatory cell infiltration and lung tissue destruction in the asthma/A(H1N1)pdm09 group than in any other group. The distinct cytokine profiles in A(H1N1)pdm09-infected asthmatic mice indicated excessive inflammation and virus replication within a few days after infection. Thus, bronchial asthma could be a more exacerbating factor for pandemic influenza infection than for seasonal influenza infection.
PMID: 28831046 DOI: 10.1038/s41598-017-08030-w