About: Transcription analysis of the porcine alveolar macrophage response to porcine circovirus type 2

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About: Transcription analysis of the porcine alveolar macrophage response to porcine circovirus type 2 Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Transcription analysis of the porcine alveolar macrophage response to porcine circovirus type 2
Creator	Chen, Huanchun He, Qigai Wang, Yang Yang, Kun Li, Wentao Charreyre, Catherine Liu, Shuqing Deng, Feng Audoneet, Jean-Christophe Yan, Weidong
Source	Medline; PMC
abstract	BACKGROUND: Porcine circovirus type 2 (PCV2) is the causal agent of postweaning multisystemic wasting syndrome (PMWS), which has severely impacted the swine industry worldwide. PCV2 triggers a weak and atypical innate immune response, but the key genes and mechanisms by which the virus interferes with host innate immunity have not yet been elucidated. In this study, genes that control the response of primary porcine alveolar macrophages (PAMs), the main target of PCV2, were profiled in vitro. RESULTS: PAMs were successfully infected by PCV2-WH strain, as evidenced quantitative real-time polymerase chain reaction (qPCR) and immunofluorescence assay (IFA) results. Infection-related differential gene expression was investigated using pig microarrays from the US Pig Genome Coordination Program and validated by real-time PCR and enzyme-linked immunosorbent assay (ELISA). Microarray analysis at 24 and 48 hours post-infection (HPI) revealed 266 and 175 unique genes, respectively, that were differentially expressed (false discovery rate <0.05; fold-change >2). Only six genes were differentially expressed between 24 and 48 HPI. The up-regulated genes were principally related to immune response, cytokine activity, locomotion, regulation of cell proliferation, apoptosis, cell growth arrest, and antigen procession and presentation. The down-regulated genes were mainly involved in terpenoid biosynthesis, carbohydrate metabolism, translation, proteasome degradation, signal transducer activity, and ribosomal proteins, which were representative of the reduced vital activity of PCV2-infected cells. CONCLUSIONS: PCV2 infection of PAMs causes up-regulation of genes related to inflammation, indicating that PCV2 may induce systematic inflammation. PCV2 persistently induced cytokines, mainly through the Toll-like receptor (TLR) 1 and TLR9 pathways, which may promote high levels of cytokine secretion. PCV2 may prevent apoptosis in PAMs by up-regulating SERPINB9 expression, possibly to lengthen the duration of PCV2 replication-permissive conditions. The observed gene expression profile may provide insights into the underlying immunological response and pathological changes that occur in pigs following PCV2 infection.
has issue date	2013-05-27(xsd:dateTime)
bibo:doi	10.1186/1471-2164-14-353
bibo:pmid	23711280
has license	cc-by
sha1sum (hex)	3498e7e96b742565d9041107cae12e667b394f9f
schema:url	https://doi.org/10.1186/1471-2164-14-353
resource representing a document's title	Transcription analysis of the porcine alveolar macrophage response to porcine circovirus type 2
has PubMed Central identifier	PMC3680065
has PubMed identifier	23711280
schema:publication	BMC Genomics
resource representing a document's body	covid:3498e7e96b742565d9041107cae12e667b394f9f#body_text
is schema:about of	named entity 'innate immune response' named entity 'swine' named entity 'alveolar' named entity 'ALVEOLAR MACROPHAGE' named entity 'PORCINE CIRCOVIRUS TYPE 2' named entity 'TARGET' named entity 'INDUSTRY' named entity 'STUDY' named entity 'AGENT' named entity 'IN VITRO' named entity 'SEVERELY' named entity 'INNATE IMMUNITY' named entity 'WEAK' named entity 'INTERFERES WITH' named entity 'TRIGGERS' named entity 'ALVEOLAR MACROPHAGES' named entity 'RESPONSE' named entity 'PORCINE' named entity 'IMPACTED' named entity 'GENES' named entity 'CONTROL' named entity 'WORLDWIDE' covid:arg/3498e7e96b742565d9041107cae12e667b394f9f named entity 'BACKGROUND' named entity 'MAIN' named entity 'PORCINE CIRCOVIRUS TYPE 2' named entity 'ANALYSIS' named entity 'TRANSCRIPTION' named entity 'HOST' named entity 'BUT' named entity 'POSTWEANING MULTISYSTEMIC WASTING SYNDROME' named entity 'INNATE IMMUNE RESPONSE' named entity 'VIRUS' named entity 'HAVE' named entity 'ATYPICAL' named entity 'RESPONSE TO' named entity 'PORCINE' named entity 'SWINE' named entity 'PRIMARY' named entity 'MECHANISMS' named entity 'KEY' named entity 'causal' named entity 'atypical' named entity 'control' named entity 'key' named entity 'virus' named entity 'alveolar macrophage' named entity 'PMWS' named entity 'porcine circovirus' named entity 'porcine' named entity 'TLR9' named entity 'PMWS' named entity 'differentially expressed' named entity 'viral replication' named entity 'Inflammatory Response' named entity 'pathogenesis' named entity 'Differentially expressed genes' named entity 'Cap protein' named entity 'Roche' named entity 'cDNA' named entity 'molecule' named entity 'Antigen Processing' named entity 'Langerhans cells' named entity 'down-regulated' named entity 'Stanford University' named entity 'Invitrogen' named entity 'peripheral blood mononuclear cells' named entity 'macrophages' named entity 'gene products' named entity 'cytokines' named entity 'Gene Cluster' named entity 'chemokine'

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