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Войти в исследования American journal of respiratory cell and molecular biology · 2026
Recurrent H1N1 Influenza A virus infections cause airway hyperinnervation and cough hypersensitivity via the IFN-γ-JAK-ERK1/2-CDK5 pathway.
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Deng Zheng, Xu Dongting, Lin Zhengyang, Ding Wenbin, Luo Mengxi, Chen Yun, Lai Kefang
Аннотация
RATIONALE: Chronic cough patients present with increased airway sensory nerve density-a pathology often initiated by recurrent viral infections, notably H1N1. Infection-induced IFN-γ acts via its highly expressed receptors to promote neurite outgrowth in vitro.
OBJECTIVES: To investigate the role of IFN-γ as a mediator in the development of airway hyperinnervation and cough hypersensitivity induced by recurrent H1N1 viral infections.
METHODS: We studied the effects and underlying mechanisms of recurrent H1N1 viral infections on airway hyperinnervation and subsequent cough hypersensitivity.
MEASUREMENTS AND MAIN RESULTS: Recurrent H1N1 viral infections in mice significantly enhanced cough sensitivity and airway inflammation, accompanied by elevated pulmonary IFN-γ + T cells/IFN-γ levels, vagal CDK5 activity, and airway nerve density. Anti-IFN-γ treatment abrogated these effects-cough hypersensitivity, IFN-γ + T cell infiltration, CDK5 upregulation, and airway hyperinnervation. Roscovitine treatment markedly attenuated viral infection-induced cough hypersensitivity, CDK5 activation in vagal ganglia, and airway hyperinnervation. Viral infections did not change gene expressions of IFN-γ receptors in vagal ganglia. Neither anti-IFN-γ nor roscovitine alleviated viral infection-induced airway inflammation. No evidence of airway hyperinnervation was observed following a single-dose H1N1 infection, either in the short term or long term. IFN-γ sensitized mouse vagal sensory neurons. Pharmacological inhibition of the JAK-ERK1/2-CDK5 pathways decreased IFN-γ-induced neurite outgrowth in mouse vagal sensory neurons.
CONCLUSIONS: Recurrent H1N1 viral infections may cause airway hyperinnervation and cough hypersensitivity via the IFN-γ-JAK-ERK1/2-CDK5 pathways. Recurrent H1N1 viral infection-induced cough hypersensitivity may be mediated, in part, by IFN-γ-mediated airway hyperinnervation.
OBJECTIVES: To investigate the role of IFN-γ as a mediator in the development of airway hyperinnervation and cough hypersensitivity induced by recurrent H1N1 viral infections.
METHODS: We studied the effects and underlying mechanisms of recurrent H1N1 viral infections on airway hyperinnervation and subsequent cough hypersensitivity.
MEASUREMENTS AND MAIN RESULTS: Recurrent H1N1 viral infections in mice significantly enhanced cough sensitivity and airway inflammation, accompanied by elevated pulmonary IFN-γ + T cells/IFN-γ levels, vagal CDK5 activity, and airway nerve density. Anti-IFN-γ treatment abrogated these effects-cough hypersensitivity, IFN-γ + T cell infiltration, CDK5 upregulation, and airway hyperinnervation. Roscovitine treatment markedly attenuated viral infection-induced cough hypersensitivity, CDK5 activation in vagal ganglia, and airway hyperinnervation. Viral infections did not change gene expressions of IFN-γ receptors in vagal ganglia. Neither anti-IFN-γ nor roscovitine alleviated viral infection-induced airway inflammation. No evidence of airway hyperinnervation was observed following a single-dose H1N1 infection, either in the short term or long term. IFN-γ sensitized mouse vagal sensory neurons. Pharmacological inhibition of the JAK-ERK1/2-CDK5 pathways decreased IFN-γ-induced neurite outgrowth in mouse vagal sensory neurons.
CONCLUSIONS: Recurrent H1N1 viral infections may cause airway hyperinnervation and cough hypersensitivity via the IFN-γ-JAK-ERK1/2-CDK5 pathways. Recurrent H1N1 viral infection-induced cough hypersensitivity may be mediated, in part, by IFN-γ-mediated airway hyperinnervation.