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iTRAQ-based quantitative proteomic analysis of peripheral blood serum in piglets infected with Actinobacillus pleuropneumoniae
Porcine pleuropneumonia caused by Actinobacillus pleuropneumoniae (APP) is a swine respiratory disease with an important impact around the world either as a single infection or part of the porcine respiratory disease complex. The data of interaction between hosts and pathogens has becoming more cruc...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer Berlin Heidelberg
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7338327/ https://www.ncbi.nlm.nih.gov/pubmed/32632500 http://dx.doi.org/10.1186/s13568-020-01057-9 |
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author | Zhu, Rining Bao, Chuntong Liu, Baijun Xiao, Jiameng Sun, Changjiang Feng, Xin Langford, P. R. Li, Yang Lei, Liancheng |
author_facet | Zhu, Rining Bao, Chuntong Liu, Baijun Xiao, Jiameng Sun, Changjiang Feng, Xin Langford, P. R. Li, Yang Lei, Liancheng |
author_sort | Zhu, Rining |
collection | PubMed |
description | Porcine pleuropneumonia caused by Actinobacillus pleuropneumoniae (APP) is a swine respiratory disease with an important impact around the world either as a single infection or part of the porcine respiratory disease complex. The data of interaction between hosts and pathogens has becoming more crucial for exploration of the mechanism. However, up to now, comparatively little information is available on the systemic and dynamic changes that occur in pig serum in response to APP infection. This study used iTRAQ to identify differentially expressed proteins (DEPs) in pig serum in response to APP infection. Compared with the APP un-infected group (S0),there were 137 up-regulated and 68 down-regulated proteins at 24 h (S24), and 81 up-regulated and 107 down-regulated proteins at 120 h (S120). At 24 h, the immune response was not significantly enriched, but cell adhesion, cytosol, Golgi apparatus, GTP and ATP binding and regulation of cell cycle were extremely active, implying host preparation of immune response starting. Subsequently, innate immune response, negative regulation of apoptotic process, immunological synapse, adaptive immune response, the regulation of inflammatory response, positive regulation of T cell proliferation were more enhanced at 120 h then that of 24 h, representing innate immunity transferring to the adaptive, while endocytosis, cell adhesion and platelet aggregation showed obvious decline. The pathways of T cell receptor signaling pathway, cytokine–cytokine receptor interaction, complement and coagulation cascades, leukocyte transendothelial migration were active remarkably during all infection period, and more pathways could connect to form innate immune defense networks. Surprisingly, the pathways like amoebiasis, rheumatoid arthritis and malaria had been found up-regulated. As a conclusion, APP could delay host inflammatory response to the infection at early stage, and induced innate immunity to convert from adhesion, interaction into complement activation, proteasome digestion, bacterial invasion at later stage. This would increase our understanding of the porcine distinct response to APP infection. |
format | Online Article Text |
id | pubmed-7338327 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Springer Berlin Heidelberg |
record_format | MEDLINE/PubMed |
spelling | pubmed-73383272020-07-09 iTRAQ-based quantitative proteomic analysis of peripheral blood serum in piglets infected with Actinobacillus pleuropneumoniae Zhu, Rining Bao, Chuntong Liu, Baijun Xiao, Jiameng Sun, Changjiang Feng, Xin Langford, P. R. Li, Yang Lei, Liancheng AMB Express Original Article Porcine pleuropneumonia caused by Actinobacillus pleuropneumoniae (APP) is a swine respiratory disease with an important impact around the world either as a single infection or part of the porcine respiratory disease complex. The data of interaction between hosts and pathogens has becoming more crucial for exploration of the mechanism. However, up to now, comparatively little information is available on the systemic and dynamic changes that occur in pig serum in response to APP infection. This study used iTRAQ to identify differentially expressed proteins (DEPs) in pig serum in response to APP infection. Compared with the APP un-infected group (S0),there were 137 up-regulated and 68 down-regulated proteins at 24 h (S24), and 81 up-regulated and 107 down-regulated proteins at 120 h (S120). At 24 h, the immune response was not significantly enriched, but cell adhesion, cytosol, Golgi apparatus, GTP and ATP binding and regulation of cell cycle were extremely active, implying host preparation of immune response starting. Subsequently, innate immune response, negative regulation of apoptotic process, immunological synapse, adaptive immune response, the regulation of inflammatory response, positive regulation of T cell proliferation were more enhanced at 120 h then that of 24 h, representing innate immunity transferring to the adaptive, while endocytosis, cell adhesion and platelet aggregation showed obvious decline. The pathways of T cell receptor signaling pathway, cytokine–cytokine receptor interaction, complement and coagulation cascades, leukocyte transendothelial migration were active remarkably during all infection period, and more pathways could connect to form innate immune defense networks. Surprisingly, the pathways like amoebiasis, rheumatoid arthritis and malaria had been found up-regulated. As a conclusion, APP could delay host inflammatory response to the infection at early stage, and induced innate immunity to convert from adhesion, interaction into complement activation, proteasome digestion, bacterial invasion at later stage. This would increase our understanding of the porcine distinct response to APP infection. Springer Berlin Heidelberg 2020-07-06 /pmc/articles/PMC7338327/ /pubmed/32632500 http://dx.doi.org/10.1186/s13568-020-01057-9 Text en © The Author(s) 2020 Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Original Article Zhu, Rining Bao, Chuntong Liu, Baijun Xiao, Jiameng Sun, Changjiang Feng, Xin Langford, P. R. Li, Yang Lei, Liancheng iTRAQ-based quantitative proteomic analysis of peripheral blood serum in piglets infected with Actinobacillus pleuropneumoniae |
title | iTRAQ-based quantitative proteomic analysis of peripheral blood serum in piglets infected with Actinobacillus pleuropneumoniae |
title_full | iTRAQ-based quantitative proteomic analysis of peripheral blood serum in piglets infected with Actinobacillus pleuropneumoniae |
title_fullStr | iTRAQ-based quantitative proteomic analysis of peripheral blood serum in piglets infected with Actinobacillus pleuropneumoniae |
title_full_unstemmed | iTRAQ-based quantitative proteomic analysis of peripheral blood serum in piglets infected with Actinobacillus pleuropneumoniae |
title_short | iTRAQ-based quantitative proteomic analysis of peripheral blood serum in piglets infected with Actinobacillus pleuropneumoniae |
title_sort | itraq-based quantitative proteomic analysis of peripheral blood serum in piglets infected with actinobacillus pleuropneumoniae |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7338327/ https://www.ncbi.nlm.nih.gov/pubmed/32632500 http://dx.doi.org/10.1186/s13568-020-01057-9 |
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