tetano
Editor, Senior Moderator
BMC Infect Dis. 2019 Jul 15;19(1):622. doi: 10.1186/s12879-019-4213-y.
[h=1]Upregulation of cell-surface mucin MUC15 in human nasal epithelial cells upon influenza A virus infection.[/h] Chen ZG[SUP]1,[/SUP][SUP]2[/SUP], Wang ZN[SUP]1,[/SUP][SUP]2[/SUP], Yan Y[SUP]2,[/SUP][SUP]3[/SUP], Liu J[SUP]2[/SUP], He TT[SUP]2[/SUP], Thong KT[SUP]2[/SUP], Ong YK[SUP]2[/SUP], Chow VTK[SUP]4[/SUP], Tan KS[SUP]5[/SUP], Wang Y[SUP]2[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] [h=4]BACKGROUND:[/h] 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.
[h=4]METHODS:[/h] 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.
[h=4]RESULTS:[/h] 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.
[h=4]CONCLUSIONS:[/h] 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.
[h=4]KEYWORDS:[/h] H3N2; Immunomodulation; MUC15; Mucin
PMID: 31307416 DOI: 10.1186/s12879-019-4213-y
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[h=1]Upregulation of cell-surface mucin MUC15 in human nasal epithelial cells upon influenza A virus infection.[/h] Chen ZG[SUP]1,[/SUP][SUP]2[/SUP], Wang ZN[SUP]1,[/SUP][SUP]2[/SUP], Yan Y[SUP]2,[/SUP][SUP]3[/SUP], Liu J[SUP]2[/SUP], He TT[SUP]2[/SUP], Thong KT[SUP]2[/SUP], Ong YK[SUP]2[/SUP], Chow VTK[SUP]4[/SUP], Tan KS[SUP]5[/SUP], Wang Y[SUP]2[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] [h=4]BACKGROUND:[/h] 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.
[h=4]METHODS:[/h] 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.
[h=4]RESULTS:[/h] 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.
[h=4]CONCLUSIONS:[/h] 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.
[h=4]KEYWORDS:[/h] H3N2; Immunomodulation; MUC15; Mucin
PMID: 31307416 DOI: 10.1186/s12879-019-4213-y
Free full text