tetano
Editor, Senior Moderator
J Exp Med. 2014 Aug 18. pii: jem.20140488. [Epub ahead of print]
Long-term survival of influenza virus infected club cells drives immunopathology.
Heaton NS1, Langlois RA2, Sachs D1, Lim JK1, Palese P3, tenOever BR4.
Author information
Abstract
Respiratory infection of influenza A virus (IAV) is frequently characterized by extensive immunopathology and proinflammatory signaling that can persist after virus clearance. In this report, we identify cells that become infected, but survive, acute influenza virus infection. We demonstrate that these cells, known as club cells, elicit a robust transcriptional response to virus infection, show increased interferon stimulation, and induce high levels of proinflammatory cytokines after successful viral clearance. Specific depletion of these surviving cells leads to a reduction in lung tissue damage associated with IAV infection. We propose a model in which infected, surviving club cells establish a proinflammatory environment aimed at controlling virus levels, but at the same time contribute to lung pathology.
? 2014 Heaton et al.
PMID:
25135297
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/25135297
Long-term survival of influenza virus infected club cells drives immunopathology.
Heaton NS1, Langlois RA2, Sachs D1, Lim JK1, Palese P3, tenOever BR4.
Author information
Abstract
Respiratory infection of influenza A virus (IAV) is frequently characterized by extensive immunopathology and proinflammatory signaling that can persist after virus clearance. In this report, we identify cells that become infected, but survive, acute influenza virus infection. We demonstrate that these cells, known as club cells, elicit a robust transcriptional response to virus infection, show increased interferon stimulation, and induce high levels of proinflammatory cytokines after successful viral clearance. Specific depletion of these surviving cells leads to a reduction in lung tissue damage associated with IAV infection. We propose a model in which infected, surviving club cells establish a proinflammatory environment aimed at controlling virus levels, but at the same time contribute to lung pathology.
? 2014 Heaton et al.
PMID:
25135297
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/25135297