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Epithelial Ion Channel Function Altered by Influenza A Induced Cytokine Production
Author(s) -
Waugh Taryn A.,
Ching John C.H.,
Glew Riley A.,
Zhou Yan,
Loewen Matthew E.
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.913.5
Subject(s) - proinflammatory cytokine , cytokine , immunology , ion channel , influenza a virus , airway , pulmonary edema , lung , biology , chemistry , medicine , virus , inflammation , receptor , anesthesia
Influenza A infection of respiratory airway epithelium produces cytokines that aid in fighting the infection. However, the excessive increase in cytokine production during severe influenza infections could contribute to altered airway ion channel activity that disrupts the airway fluid balance leading to pulmonary edema. Using qRT‐PCR and Bio‐Plex array we measured cytokines in Calu‐3 cells infected with influenza A. We simultaneously measured channel function by means of short‐circuit current produced by a Calu‐3 monolayer in response to agonists and channel blockers. Viral protein production and initial increases in cytokines were found at 24 hours post infection. Interestingly, no change in short‐circuit current response was found. However, further increases in proinflammatory cytokines at 48 hours post infection, such as IL‐8 and IL‐6, did correlate with a change in the agonist induced short‐circuit current response. However, the observed decreases in cAMP induced short‐circuit current, did not correlate with the significant increases in CFTR mRNA. In conclusion, influenza infection either directly or in concert with cytokines can induce transcriptional expression of ion channels but simultaneously inhibit their function. This study helps understand the pathophysiology which drives fluid into the lungs during an influenza A infection. Support: SHRF, EHRF, CAHF, CFI and NSERC