Progranulin (PGRN) exerts multiple functions in various inflammatory diseases. However, the role of PGRN in the pathogenesis of virus infection is unknown. Here, we demonstrated that PGRN production was up-regulated in clinical and experimental influenza, which contributed to the deleterious inflammatory response after influenza virus infection in mice. PGRN-deficient mice were protected from influenza virus-induced lung injury and mortality. Decreased mortality was associated with significantly reduced influx of neutrophils and monocytes/macrophages, release of cytokines and chemokines, and permeability of the alveolar–epithelial barrier without affecting viral clearance. Our findings suggest that PGRN exacerbates pulmonary immunopathology during influenza virus infection.
- viral infection
- infection control
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Contributors Conception hypothesis and design: JC and YY; data acquisition and analysis: QL, XY, HT, JC and YY; manuscript preparation: JC and QL.
Funding This work was supported by National Natural Science Foundation of China grants 81722001 and 81572038 (to JC), and Chongqing Science and Technology Commission Grant for Distinguished Young Scholars of Chongqing (grant number, cstc2014jcyjjq10002) (to JC).
Competing interests None declared.
Patient consent Obtained.
Ethics approval Clinical Research Ethics Committee of The First Affiliated Hospital of Chongqing Medical University.
Provenance and peer review Not commissioned; externally peer reviewed.
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