tetano
Editor, Senior Moderator
Exp Cell Res. 2018 Aug 21. pii: S0014-4827(18)30757-2. doi: 10.1016/j.yexcr.2018.08.022. [Epub ahead of print]
[h=1]H3N2 influenza virus infection enhances Oncostatin M expression in human nasal epithelium.[/h] Tian T[SUP]1[/SUP], Zi X[SUP]2[/SUP], Peng Y[SUP]3[/SUP], Wang Z[SUP]4[/SUP], Hong H[SUP]5[/SUP], Yan Y[SUP]5[/SUP], Guan W[SUP]6[/SUP], Tan KS[SUP]7[/SUP], Liu J[SUP]7[/SUP], Ong HH[SUP]7[/SUP], Kang X[SUP]8[/SUP], Yu J[SUP]8[/SUP], Ong YK[SUP]7[/SUP], Thong KT[SUP]7[/SUP], Shi L[SUP]7[/SUP], Ye J[SUP]9[/SUP], Wang DY[SUP]10[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Tight junctions (TJs) alteration is commonly seen in airway inflammatory diseases. Oncostatin M (OSM) is an inflammatory mediator associated with chronic rhinosinusitis with nasal polyps (CRSwNP). We have previously shown that human nasal epithelial cells (hNECs) are highly permissive cells for influenza A virus (IAV). However, its role in TJs alteration and the effects of IAV on inducing OSM expression in nasal epithelium remains to be further investigated. In this study, OSM and TJs expression was measured and compared between inferior turbinate from healthy controls and nasal polyps from CRSwNP. Additionally, hNECs cultured at air-liquid interface (ALI) were infected with H3N2 influenza virus to study the role of influenza virus in inducing epithelial OSM expression as a possible means of exacerbation. The expression of ZO-1, claudin-1, and occludin was markedly decreased and correlated negatively with that of OSM in CRSwNP. By using the in vitro hNEC model, H3N2 infection resulted in significantly increased OSM expression (2.2-, 4.7- and 3.9-fold higher at 8, 24, and 48hours post-infection vs. mock infection). Furthermore, OSM is found to co-localize with ciliated and goblet cells in hNECs infected with H3N2 influenza virus. Our findings demonstrated that increased OSM expression is implicated in CRSwNP as a possible mechanism of TJs' impairment, which can be further augmented following influenza infection via epithelial OSM expression, possibly contributing to exacerbations.
[h=4]KEYWORDS:[/h] Oncostatin M; chronic rhinosinusitis with nasal polyps; influenza A; tight junctions; viral exacerbation
PMID: 30142324 DOI: 10.1016/j.yexcr.2018.08.022
[h=1]H3N2 influenza virus infection enhances Oncostatin M expression in human nasal epithelium.[/h] Tian T[SUP]1[/SUP], Zi X[SUP]2[/SUP], Peng Y[SUP]3[/SUP], Wang Z[SUP]4[/SUP], Hong H[SUP]5[/SUP], Yan Y[SUP]5[/SUP], Guan W[SUP]6[/SUP], Tan KS[SUP]7[/SUP], Liu J[SUP]7[/SUP], Ong HH[SUP]7[/SUP], Kang X[SUP]8[/SUP], Yu J[SUP]8[/SUP], Ong YK[SUP]7[/SUP], Thong KT[SUP]7[/SUP], Shi L[SUP]7[/SUP], Ye J[SUP]9[/SUP], Wang DY[SUP]10[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] Tight junctions (TJs) alteration is commonly seen in airway inflammatory diseases. Oncostatin M (OSM) is an inflammatory mediator associated with chronic rhinosinusitis with nasal polyps (CRSwNP). We have previously shown that human nasal epithelial cells (hNECs) are highly permissive cells for influenza A virus (IAV). However, its role in TJs alteration and the effects of IAV on inducing OSM expression in nasal epithelium remains to be further investigated. In this study, OSM and TJs expression was measured and compared between inferior turbinate from healthy controls and nasal polyps from CRSwNP. Additionally, hNECs cultured at air-liquid interface (ALI) were infected with H3N2 influenza virus to study the role of influenza virus in inducing epithelial OSM expression as a possible means of exacerbation. The expression of ZO-1, claudin-1, and occludin was markedly decreased and correlated negatively with that of OSM in CRSwNP. By using the in vitro hNEC model, H3N2 infection resulted in significantly increased OSM expression (2.2-, 4.7- and 3.9-fold higher at 8, 24, and 48hours post-infection vs. mock infection). Furthermore, OSM is found to co-localize with ciliated and goblet cells in hNECs infected with H3N2 influenza virus. Our findings demonstrated that increased OSM expression is implicated in CRSwNP as a possible mechanism of TJs' impairment, which can be further augmented following influenza infection via epithelial OSM expression, possibly contributing to exacerbations.
[h=4]KEYWORDS:[/h] Oncostatin M; chronic rhinosinusitis with nasal polyps; influenza A; tight junctions; viral exacerbation
PMID: 30142324 DOI: 10.1016/j.yexcr.2018.08.022