Background Cell-surface mucins are expressed in apical epithelial cells of the respiratory tract, and contribute a crucial part of the innate immune system. Despite anti-inflammatory or antiviral functions being revealed for certain cell-surface mucins such as MUC1, the roles of other mucins are still poorly understood, especially in viral infections. Methods To further identify mucins significant in influenza infection, we screened the expression of mucins in human nasal epithelial cells infected by H3N2 influenza A virus. Results We found that the expression of MUC15 was significantly upregulated upon infection, and specific only to active infection. While MUC15 did not interact with virus particles or reduce viral replication directly, positive correlations were observed between MUC15 and inflammatory factors in response to viral infection. Given that the upregulation of MUC15 was only triggered late into infection when immune factors (including cytokines, chemokines, EGFR and phosphorylated ERK) started to peak and plateau, MUC15 may potentially serve an immunomodulatory function later during influenza viral infection. Conclusions Our study revealed that MUC15 was one of the few cell-surface mucins induced during influenza infection. While MUC15 did not interact directly with influenza virus, we showed that its increase coincides with the peak of immune activation and thus MUC15 may serve an immunomodulatory role during influenza infection. Electronic supplementary material The online version of this article (10.1186/s12879-019-4213-y) contains supplementary material, which is available to authorized users.

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Idiopathic pulmonary fibrosis (IPF) is a chronic lung disease of unknown etiology and high mortality. Current therapeutic strategies have limited efficacy and the prognosis remains poor. Based on the histological observations of IPF lung tissues and experimental studies using lung fibrosis animal models, it is gradually accepted that impaired epithelial regeneration after lung injury is a critical mechanism underlying the pathogenesis of pulmonary fibrosis. The central role of AEC2 in this process has been well-elucidated, while the contribution of other lung progenitor/stem cells is less discussed. Recently, increasing studies have identified several non-AEC2 epithelial progenitor/stem cells with great plasticity to transform into mature AECs and reconstitute alveolar epithelium after lung injury. However, why these cells do not function as alternate stem cells to regenerate alveolar epithelium in IPF is still unknown. In this review, we discuss the contribution of lung epithelial progenitor/stem cells in the aberrant alveolar regeneration, and provide a novel perspective on the mechanism of IPF pathogenesis, in which non-AEC2 progenitors may play an essential role.