Lethal Dissemination of H5N1 Influenza Virus Is Associated with Dysregulation of Inflammation and Lipoxin Signaling in a Mouse Model of Infection

Cillóniz, Cristian; Pantin‐Jackwood, Mary J.; Ni, Chester; Goodman, Alan G.; Peng, Xinxia; Proll, Sean; Carter, Victoria S.; Rosenzweig, Elizabeth; Szretter, Kristy J.; Katz, Jacqueline M.; Korth, Marcus J.; Swayne, David E.; Tumpey, Terrence M.; Katze, Michael G.

doi:10.1128/jvi.00553-10

Cited by 125 publications

(122 citation statements)

References 44 publications

(42 reference statements)

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“…These results further suggest that mast cells are involved in the pathogenesis of H5N1 virus infection and that preventing aberrant inflammation could protect the mice from mortality. Previous studies reported that cytokine dysregulation contributed to the severity of influenza H5N1 virus infection 39, 40. Consistent with those, the current results in our report further support that an atypical immune response, rather than uncontrollable virus replication, resulted in acute mortality after highly pathogenic H5N1 virus infection.…”

Section: Discussionsupporting

confidence: 92%

The therapeutic effects of sodium cromoglycate against influenza A virus H5N1 in mice

Han

Wei

Zhang

et al. 2015

Influenza Resp Viruses

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ObjectivesTo identify the protective role of sodium cromoglycate in mice during influenza virus infection.DesignH5N1 virus‐infected mice were treated with the mast cell stabilizer sodium cromoglycate (SCG) to investigate its therapeutic effect.SampleThe nose, trachea and lungs from mice were collected.Main outcome measuresVirus replication and host responses were determined by plaque assay, quantitative PCR, immunohistochemistry, and histology.ResultsSCG‐treated mice survived better than did PBS‐treated mice after H5N1 virus infection. Mild pathological changes with fewer inflammatory cell infiltration and fewer virus antigens were observed in the nose, trachea, and lungs of SCG‐treated mice on days 3 and 5 post‐infection. However, no significant changes in viral load in the lungs were detected between SCG‐ and PBS‐treated mice. Furthermore, significantly decreased expression of interleukin‐6, tumor necrosis factor‐a, Toll‐like receptor 3, and TIR‐domain‐containing adapter‐inducing interferon‐b was detected in the lungs of SCG‐treated mice, and no higher expression of interferon‐c was detected.ConclusionThese results suggest that SCG has therapeutic roles in H5N1 virus‐infected mice by alleviating the inflammatory response rather than inhibition of viral replication in the lungs.

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Section: Discussionsupporting

confidence: 92%

The therapeutic effects of sodium cromoglycate against influenza A virus H5N1 in mice

Han

Wei

Zhang

et al. 2015

Influenza Resp Viruses

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“…The microarray data are available at GEO accession number GSE76719. Similar to previous studies, influenza virus infection dramatically changed the overall expression pattern in host cells (17,18). The expression of hundreds of genes was highly upregulated or downregulated compared with AF.…”

Section: Resultssupporting

confidence: 81%

FAT10 Is Critical in Influenza A Virus Replication by Inhibiting Type I IFN

Tang

Yang

Liu

et al. 2016

The Journal of Immunology

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The H5N1 avian influenza virus causes severe disease and high mortality, making it a major public health concern worldwide. The virus uses the host cellular machinery for several steps of its life cycle. In this report, we observed overexpression of the ubiquitin-like protein FAT10 following live H5N1 virus infection in BALB/c mice and in the human respiratory epithelial cell lines A549 and BEAS-2B. Further experiments demonstrated that FAT10 increased H5N1 virus replication and decreased the viability of infected cells. Total RNA extracted from H5N1 virus–infected cells, but not other H5N1 viral components, upregulated FAT10, and this process was mediated by the retinoic acid–induced protein I-NF-κB signaling pathway. FAT10 knockdown in A549 cells upregulated type I IFN mRNA expression and enhanced STAT1 phosphorylation during live H5N1 virus infection. Taken together, our data suggest that FAT10 was upregulated via retinoic acid–induced protein I and NF-κB during H5N1 avian influenza virus infection. And the upregulated FAT10 promoted H5N1 viral replication by inhibiting type I IFN.

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“…It has been proposed that excessive or dysregulated lung infl ammation is responsible for infl uenza-induced mortality [30,31]. Cilloniz et al [30] have showed that virus type H5N1 VN/1203 is more lethal than the H1N1 1918 pandemic virus in mice even though there was no difference in lung virus titers; however the greater lethality of H5N1 VN/1203 was associated with an earlier and stronger inflammatory response and a down-regulated anti-infl ammatory response.…”

Section: Discussionmentioning

confidence: 99%

“…Cilloniz et al [30] have showed that virus type H5N1 VN/1203 is more lethal than the H1N1 1918 pandemic virus in mice even though there was no difference in lung virus titers; however the greater lethality of H5N1 VN/1203 was associated with an earlier and stronger inflammatory response and a down-regulated anti-infl ammatory response. Therefore, it seems that the inflammatory response has an important effect on the symptoms and lethality of infl uenza virus infection.…”

Section: Discussionmentioning

confidence: 99%

Effect of Oral Administration of Korean Red Ginseng on Influenza A (H1N1) Virus Infection

Kim¹,

Kim²,

Kim

2011

Journal of Ginseng Research

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Korean red ginseng (RG), which is a ginseng treated by heating and steaming, has biological activity similar to Panax ginseng. The effect of ginseng on influenza infection has not been studied although it is known to have a broad range of biological activities. The aim of the study is to investigate the effect of RG extract on infl uenza A (H1N1) virus infection. We investigated the inhibitory effect of RG extract on plaque formation by infl uenza A virus in a cell-based plaque assay, and the effect of orally administered RG on infl uenza A virus infection in mice. RG extract, which was applied at a non-cytotoxic concentration, inhibited plaque formation by infl uenza A virus in the cell-based plaque assay. The orally administered RG extract ameliorated body weight loss and signifi cantly increased survival in mice infected with infl uenza A virus. Our results suggest that RG extract has components that reduce the severity of infection by infl uenza A virus and could potentially be used as a complement to treatment of infl uenza A virus infections.

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Lethal Dissemination of H5N1 Influenza Virus Is Associated with Dysregulation of Inflammation and Lipoxin Signaling in a Mouse Model of Infection

Cited by 125 publications

References 44 publications

The therapeutic effects of sodium cromoglycate against influenza A virus H5N1 in mice

The therapeutic effects of sodium cromoglycate against influenza A virus H5N1 in mice

FAT10 Is Critical in Influenza A Virus Replication by Inhibiting Type I IFN

Effect of Oral Administration of Korean Red Ginseng on Influenza A (H1N1) Virus Infection

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