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Open Access Highly Accessed Research article

Effect of avian influenza A H5N1 infection on the expression of microRNA-141 in human respiratory epithelial cells

Wai-Yip Lam1, Apple Chung-Man Yeung2, Karry Lei-Ka Ngai2, Man-Shan Li1, Ka-Fai To3, Stephen Kwok-Wing Tsui1 and Paul Kay-Sheung Chan24*

Author Affiliations

1 School of Biomedical Sciences, Faculty of Medicine, The Chinese University of Hong Kong, New Territories, Hong Kong Special Administration Region, Shatin, People’s Republic of China

2 Departments of Microbiology, Faculty of Medicine, The Chinese University of Hong Kong, Prince of Wales Hospital, New Territories, Hong Kong Special Administration Region, Shatin, People’s Republic of China

3 Department of Anatomical and Cellular Pathology, Faculty of Medicine, The Chinese University of Hong Kong, Prince of Wales Hospital, New Territories, Hong Kong Special Administration Region, Shatin, People’s Republic of China

4 Stanley Ho Centre for Emerging Infectious Diseases, Faculty of Medicine, The Chinese University of Hong Kong, Prince of Wales Hospital, New Territories, Hong Kong Special Administration Region, Shatin, People’s Republic of China

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BMC Microbiology 2013, 13:104  doi:10.1186/1471-2180-13-104

Published: 10 May 2013

Abstract

Background

Avian influenza remains a serious threat to human health. The consequence of human infection varies markedly among different subtypes of avian influenza viruses. In addition to viral factors, the difference in host cellular response is likely to play a critical role. This study aims at elucidating how avian influenza infection perturbs the host’s miRNA regulatory pathways that may lead to adverse pathological events, such as cytokine storm, using the miRNA microarray approach.

Results

The results showed that dysregulation of miRNA expression was mainly observed in highly pathogenic avian influenza A H5N1 infection. We found that miR-21*, miR-100*, miR-141, miR-574-3p, miR-1274a and miR1274b were differentially expressed in response to influenza A virus infection. Interestingly, we demonstrated that miR-141, which was more highly induced by H5N1 than by H1N1 (p < 0.05), had an ability to suppress the expression of a cytokine - transforming growth factor (TGF)-β2. This was supported by the observation that the inhibitory effect could be reversed by antagomiR-141.

Conclusions

Since TGF-β2 is an important cytokine that can act as both an immunosuppressive agent and a potent proinflammatory molecule through its ability to attract and regulate inflammatory molecules, and previous report showed that only seasonal influenza H1N1 (but not the other avian influenza subtypes) could induce a persistent expression of TGF-β2, we speculate that the modulation of TGF-β2 expression by different influenza subtypes via miR-141 might be a critical step for determining the outcome of either normal or excessive inflammation progression.

Keywords:
microRNA; Influenza A virus; H1N1; H5N1; Inflammation; Hypercytokinemia; Pathogenesis