serval:BIB_DDD8EF9FDA5F
Targeting IL-1β and IL-17A driven inflammation during influenza-induced exacerbations of chronic lung inflammation.
10.1371/journal.pone.0098440
000338631000017
24918427
Sichelstiel
A.
author
Yadava
K.
author
Trompette
A.
author
Salami
O.
author
Iwakura
Y.
author
Nicod
L.P.
author
Marsland
B.J.
author
article
2014
Plos One
1932-6203
1932-6203
journal
9
6
e98440
For patients with chronic lung diseases, such as chronic obstructive pulmonary disease (COPD), exacerbations are life-threatening events causing acute respiratory distress that can even lead to hospitalization and death. Although a great deal of effort has been put into research of exacerbations and potential treatment options, the exact underlying mechanisms are yet to be deciphered and no therapy that effectively targets the excessive inflammation is available. In this study, we report that interleukin-1β (IL-1β) and interleukin-17A (IL-17A) are key mediators of neutrophilic inflammation in influenza-induced exacerbations of chronic lung inflammation. Using a mouse model of disease, our data shows a role for IL-1β in mediating lung dysfunction, and in driving neutrophilic inflammation during the whole phase of viral infection. We further report a role for IL-17A as a mediator of IL-1β induced neutrophilia at early time points during influenza-induced exacerbations. Blocking of IL-17A or IL-1 resulted in a significant abrogation of neutrophil recruitment to the airways in the initial phase of infection or at the peak of viral replication, respectively. Therefore, IL-17A and IL-1β are potential targets for therapeutic treatment of viral exacerbations of chronic lung inflammation.
eng
60_published
true
peer-reviewed
Publication types: Journal Article ; Research Support, Non-U.S. Gov'tPublication Status: epublish
University of Lausanne
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