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Transcription analysis on response of swine lung to H1N1 swine influenza virus
BACKGROUND: As a mild, highly contagious, respiratory disease, swine influenza always damages the innate immune systems, and increases susceptibility to secondary infections which results in considerable morbidity and mortality in pigs. Nevertheless, the systematical host response of pigs to swine i...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2011
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3169531/ https://www.ncbi.nlm.nih.gov/pubmed/21819625 http://dx.doi.org/10.1186/1471-2164-12-398 |
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author | Li, Yongtao Zhou, Hongbo Wen, Zhibin Wu, Shujuan Huang, Canhui Jia, Guangmin Chen, Huanchun Jin, Meilin |
author_facet | Li, Yongtao Zhou, Hongbo Wen, Zhibin Wu, Shujuan Huang, Canhui Jia, Guangmin Chen, Huanchun Jin, Meilin |
author_sort | Li, Yongtao |
collection | PubMed |
description | BACKGROUND: As a mild, highly contagious, respiratory disease, swine influenza always damages the innate immune systems, and increases susceptibility to secondary infections which results in considerable morbidity and mortality in pigs. Nevertheless, the systematical host response of pigs to swine influenza virus infection remains largely unknown. To explore it, a time-course gene expression profiling was performed for comprehensive analysis of the global host response induced by H1N1 swine influenza virus in pigs. RESULTS: At the early stage of H1N1 swine virus infection, pigs were suffering mild respiratory symptoms and pathological changes. A total of 268 porcine genes showing differential expression (DE) after inoculation were identified to compare with the controls on day 3 post infection (PID) (Fold change ≥ 2, p < 0.05). The DE genes were involved in many vital functional classes, mainly including signal transduction, immune response, inflammatory response, cell adhesion and cell-cell signalling. Noticeably, the genes associated with immune and inflammatory response showed highly overexpressed. Through the pathway analysis, the significant pathways mainly concerned with Cell adhesion molecules, Cytokine-cytokine receptor interaction, Toll-like receptor signaling pathway and MAPK signaling pathway, suggesting that the host took different strategies to activate these pathways so as to prevent virus infections at the early stage. However, on PID 7, the predominant function classes of DE genes included signal transduction, metabolism, transcription, development and transport. Furthermore, the most significant pathways switched to PPAR signaling pathway and complement and coagulation cascades, showing that the host might start to repair excessive tissue damage by anti-inflammatory functions. These results on PID 7 demonstrated beneficial turnover for host to prevent excessive inflammatory damage and recover the normal state by activating these clusters of genes. CONCLUSIONS: This study shows how the target organ responds to H1N1 swine influenza virus infection in pigs. The observed gene expression profile could help to screen the potential host agents for reducing the prevalence of swine influenza virus and further understand the molecular pathogenesis associated with H1N1 infection in pigs. |
format | Online Article Text |
id | pubmed-3169531 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2011 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-31695312011-09-09 Transcription analysis on response of swine lung to H1N1 swine influenza virus Li, Yongtao Zhou, Hongbo Wen, Zhibin Wu, Shujuan Huang, Canhui Jia, Guangmin Chen, Huanchun Jin, Meilin BMC Genomics Research Article BACKGROUND: As a mild, highly contagious, respiratory disease, swine influenza always damages the innate immune systems, and increases susceptibility to secondary infections which results in considerable morbidity and mortality in pigs. Nevertheless, the systematical host response of pigs to swine influenza virus infection remains largely unknown. To explore it, a time-course gene expression profiling was performed for comprehensive analysis of the global host response induced by H1N1 swine influenza virus in pigs. RESULTS: At the early stage of H1N1 swine virus infection, pigs were suffering mild respiratory symptoms and pathological changes. A total of 268 porcine genes showing differential expression (DE) after inoculation were identified to compare with the controls on day 3 post infection (PID) (Fold change ≥ 2, p < 0.05). The DE genes were involved in many vital functional classes, mainly including signal transduction, immune response, inflammatory response, cell adhesion and cell-cell signalling. Noticeably, the genes associated with immune and inflammatory response showed highly overexpressed. Through the pathway analysis, the significant pathways mainly concerned with Cell adhesion molecules, Cytokine-cytokine receptor interaction, Toll-like receptor signaling pathway and MAPK signaling pathway, suggesting that the host took different strategies to activate these pathways so as to prevent virus infections at the early stage. However, on PID 7, the predominant function classes of DE genes included signal transduction, metabolism, transcription, development and transport. Furthermore, the most significant pathways switched to PPAR signaling pathway and complement and coagulation cascades, showing that the host might start to repair excessive tissue damage by anti-inflammatory functions. These results on PID 7 demonstrated beneficial turnover for host to prevent excessive inflammatory damage and recover the normal state by activating these clusters of genes. CONCLUSIONS: This study shows how the target organ responds to H1N1 swine influenza virus infection in pigs. The observed gene expression profile could help to screen the potential host agents for reducing the prevalence of swine influenza virus and further understand the molecular pathogenesis associated with H1N1 infection in pigs. BioMed Central 2011-08-08 /pmc/articles/PMC3169531/ /pubmed/21819625 http://dx.doi.org/10.1186/1471-2164-12-398 Text en Copyright ©2011 Li et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Li, Yongtao Zhou, Hongbo Wen, Zhibin Wu, Shujuan Huang, Canhui Jia, Guangmin Chen, Huanchun Jin, Meilin Transcription analysis on response of swine lung to H1N1 swine influenza virus |
title | Transcription analysis on response of swine lung to H1N1 swine influenza virus |
title_full | Transcription analysis on response of swine lung to H1N1 swine influenza virus |
title_fullStr | Transcription analysis on response of swine lung to H1N1 swine influenza virus |
title_full_unstemmed | Transcription analysis on response of swine lung to H1N1 swine influenza virus |
title_short | Transcription analysis on response of swine lung to H1N1 swine influenza virus |
title_sort | transcription analysis on response of swine lung to h1n1 swine influenza virus |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3169531/ https://www.ncbi.nlm.nih.gov/pubmed/21819625 http://dx.doi.org/10.1186/1471-2164-12-398 |
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