Angiopoietin-like 4 Increases Pulmonary Tissue Leakiness and Damage during Influenza Pneumonia

Li, Liang; Chong, Han Chung; Ng, Say Yong; Kwok, Ka Wai; Teo, Ziqiang; Tan, Eddie Han Pin; Choo, Chee Chong; Seet, Ju Ee; Choi, Hyungwon; Buist, Martin L.; Chow, Vincent T. K.; Tan, Nguan Soon

doi:10.1016/j.celrep.2015.01.011

Cited by 67 publications

(84 citation statements)

References 29 publications

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“…In addition, ANGPTL4, which has been implicated in IAV infection (Li et al, 2015), was also among the validated antiviral factors. Furthermore, we identified CCL3L3, a cytokine that binds to several chemokine receptors, including CCR5, and acts as a chemotactic for lymphocytes and monocytes.…”

Section: Resultsmentioning

confidence: 99%

Meta- and Orthogonal Integration of Influenza “OMICs” Data Defines a Role for UBR4 in Virus Budding

Tripathi

Pohl

Zhou

et al. 2015

Cell Host & Microbe

831

724

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SUMMARY Several systems-level datasets designed to dissect host-pathogen interactions during influenza A infection have been reported. However, apparent discordance among these data has hampered their full utility toward advancing mechanistic and therapeutic knowledge. To collectively reconcile these datasets, we performed a meta-analysis of data from eight published RNAi screens and integrated these data with three protein interaction datasets, including one generated within the context of this study. Further integration of these data with global virus-host interaction analyses revealed a functionally validated biochemical landscape of the influenza-host interface, which can be queried through a simplified and customizable web portal (http://www.metascape.org/IAV). Follow-up studies revealed that the putative ubiquitin ligase UBR4 associates with the viral M2 protein and promotes apical transport of viral proteins. Taken together, the integrative analysis of influenza OMICs datasets illuminates a viral-host network of high-confidence human proteins that are essential for influenza A virus replication.

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Section: Resultsmentioning

confidence: 99%

Meta- and Orthogonal Integration of Influenza “OMICs” Data Defines a Role for UBR4 in Virus Budding

Tripathi

Pohl

Zhou

et al. 2015

Cell Host & Microbe

831

724

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“…Nevertheless, the increased infiltration of immune cells and heightened inflammation did not cause increased cytotoxicity in T-bet À/À lungs as reflected by the level of lactate dehydrogenase (LDH) in the BAL (Fig 1E). To further assess tissue repair in T-bet À/À lungs, podoplanin (PDPN), a glycoprotein expressed on alveolar type 1 epithelial cells and marker of lung injury and repair (Li et al, 2015;Zuo et al, 2015), was stained by Western blot (Figs 1F and EV1D) and immunohistochemistry (Fig EV1E). To further assess tissue repair in T-bet À/À lungs, podoplanin (PDPN), a glycoprotein expressed on alveolar type 1 epithelial cells and marker of lung injury and repair (Li et al, 2015;Zuo et al, 2015), was stained by Western blot (Figs 1F and EV1D) and immunohistochemistry (Fig EV1E).…”

Section: T-bet à/à Mice Clear Influenza Virus Infection With Increasementioning

confidence: 99%

Loss of T‐bet confers survival advantage to influenza–bacterial superinfection

Koean

Ding

2018

The EMBO Journal

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The transcription factor, T‐bet, regulates type 1 inflammatory responses against a range of infections. Here, we demonstrate a previously unaddressed role of T‐bet, to influenza virus and bacterial superinfection. Interestingly, we found that T‐bet deficiency did not adversely affect the efficacy of viral clearance or recovery compared to wild‐type hosts. Instead, increased infiltration of neutrophils and production of Th17 cytokines (IL‐17 and IL‐22), in lungs of influenza virus‐infected T‐bet−/− mice, were correlated with survival advantage against subsequent infection by Streptococcus pneumoniae. Neutralization of IL‐17, but not IL‐22, in T‐bet−/− mice increased pulmonary bacterial load, concomitant with decreased neutrophil infiltration and reduced survival of T‐bet−/− mice. IL‐17 production by CD8+, CD4+ and γδ T cell types was identified to contribute to this protection against bacterial superinfection. We further showed that neutrophil depletion in T‐bet−/− lungs increased pulmonary bacterial burden. These results thus indicate that despite the loss of T‐bet, immune defences required for influenza viral clearance are fully functional, which in turn enhances protective type 17 immune responses against lethal bacterial superinfections.

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“…We chose ANGPTL4 for further analysis, because its expression could be induced by acute phase response [31]. Liang et al [32] showed that influenza infection could stimulate the expression of ANGPTL4, and treatment of infected mice with neutralizing anti-ANGPTL4 antibodies significantly accelerated lung recovery and improved lung tissue integrity. Moreover, ANGPTL4-deficient mice also showed reduced lung damage and recovered faster from influenza infection when compared to their wild-type counterparts.…”

Section: Discussionmentioning

confidence: 99%

Effect of Maxing Shigan Tang on H1N1 Influenza A Virus-Associated Acute Lung Injury in Mice

et al. 2016

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Objective: This study is aimed at examining the effects of Maxing Shigan Tang (MST) treatment on H1N1-associated acute lung injury (ALI) and exploring the possible mechanism. Material and Methods: Mice were randomly divided into a control group, model group, peroxisomal proliferator activator receptor γ (PPARγ) inhibition group (PPARγ-), PPARγ activation group (PPARγ+), and MST group. Influenza A (H1N1) virus of the Fort Monmouth 1 (FM1) strain was used to induce an ALI mice model. Hematoxylin and eosin staining was performed to investigate the effect of MST treatment on H1N1-associated ALI. Cell apoptosis of lung tissues of each group were conducted through transferase-mediated dUTP nick end-labeling methods. Moreover, the expression level of caspase 3, activity of caspase 3, and serum level of tumor necrosis factor (TNF)-α of each group were also analyzed. Finally, quantitative real-time polymerase chain reaction and Western blotting analysis were carried out to detect angiopoietin-like 4 (ANGPTL4) expression level. Results: We found that mice infected with the FM1 strain of H1N1 influenza A virus developed severe ALI, and MST could improve H1N1-induced ALI. Moreover, MST decreased lung cell apoptosis and reduced the serum content of TNF-α. In addition, MST significantly induced the ANGPTL4 expression in H1N1-induced ALI. Conclusion: MST improves H1N1-associated ALI maybe through targeting ANGPTL4 in mice.

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Angiopoietin-like 4 Increases Pulmonary Tissue Leakiness and Damage during Influenza Pneumonia

Cited by 67 publications

References 29 publications

Meta- and Orthogonal Integration of Influenza “OMICs” Data Defines a Role for UBR4 in Virus Budding

Meta- and Orthogonal Integration of Influenza “OMICs” Data Defines a Role for UBR4 in Virus Budding

Loss of T‐bet confers survival advantage to influenza–bacterial superinfection

Effect of Maxing Shigan Tang on H1N1 Influenza A Virus-Associated Acute Lung Injury in Mice

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