Type 2 porcine reproductive and respiratory syndrome virus infection increases apoptosis at the maternal-fetal interface in late gestation pregnant gilts
The pathogenesis of fetal death associated with porcine reproductive and respiratory syndrome (PRRS) is hypothesized to be a consequence of PRRS virus-induced apoptosis at the maternal-fetal interface (MFI). The objectives of this study were to evaluate distribution and degree of apoptosis in the ut...
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description | The pathogenesis of fetal death associated with porcine reproductive and respiratory syndrome (PRRS) is hypothesized to be a consequence of PRRS virus-induced apoptosis at the maternal-fetal interface (MFI). The objectives of this study were to evaluate distribution and degree of apoptosis in the uterine and fetal placental tissues during the experimental type 2 PRRS virus (PRRSV) infection and determine associations between apoptosis at the MFI, PRRSV RNA concentration and antigen staining intensity, PRRSV-induced microscopic lesions, and fetal preservation status. A total of 114 naïve, high-health pregnant gilts were inoculated with type 2 PRRSV on gestation day 85±1 with euthanasia 21 days later; 19 sham-inoculated gilts served as controls. Two hundred and fifty samples of uterine tissue with fetal placenta were selected based on negative, low PRRSV RNA, and high PRRSV RNA concentration (0, < or > 2.7 log10 copies/mg, respectively). TUNEL assay was used to detect apoptosis in the endometrium and at the MFI. PRRSV RNA concentration and numbers of PRRSV immunopositive cells in uterine and placental tissue were positively associated with the severity of apoptosis in the endometrium and the MFI (P |
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The objectives of this study were to evaluate distribution and degree of apoptosis in the uterine and fetal placental tissues during the experimental type 2 PRRS virus (PRRSV) infection and determine associations between apoptosis at the MFI, PRRSV RNA concentration and antigen staining intensity, PRRSV-induced microscopic lesions, and fetal preservation status. A total of 114 naïve, high-health pregnant gilts were inoculated with type 2 PRRSV on gestation day 85±1 with euthanasia 21 days later; 19 sham-inoculated gilts served as controls. Two hundred and fifty samples of uterine tissue with fetal placenta were selected based on negative, low PRRSV RNA, and high PRRSV RNA concentration (0, < or > 2.7 log10 copies/mg, respectively). TUNEL assay was used to detect apoptosis in the endometrium and at the MFI. PRRSV RNA concentration and numbers of PRRSV immunopositive cells in uterine and placental tissue were positively associated with the severity of apoptosis in the endometrium and the MFI (P<0.001, P<0.05 and P<0.001, respectively). The number of TUNEL positive cells at the MFI was also positively associated with the severity (P<0.001) of vasculitis, but not total numbers of inflammatory cells in the endometrium. Increased numbers of TUNEL positive cells at the MFI were associated with PRRSV load in the fetal thymus, and greater odds of meconium staining of the fetus at 21 days post infection (P<0.001 for both). These findings suggest an important role of apoptosis in the pathogenesis of uterine epithelial and trophoblastic cell death at the MFI. Moreover, apoptosis at the MFI is significantly associated with fetal demise during in utero type 2 PRRSV infection.]]></description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0173360</identifier><identifier>PMID: 28253336</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Analysis ; Animals ; Apoptosis ; Biology and Life Sciences ; Cell death ; Endometrium ; Euthanasia ; Female ; Fetuses ; Genetic aspects ; Gestation ; Health aspects ; In Situ Nick-End Labeling ; Infections ; Inflammation ; Lesions ; Maternal-Fetal Exchange ; Meconium ; Medicine and Health Sciences ; Pathogenesis ; Pathology ; Placenta ; Placenta - metabolism ; Placenta - virology ; Porcine reproductive and respiratory syndrome ; Porcine Reproductive and Respiratory Syndrome - pathology ; Porcine respiratory and reproductive syndrome virus ; Porcine respiratory and reproductive syndrome virus - genetics ; Porcine respiratory and reproductive syndrome virus - pathogenicity ; Pregnancy ; Pregnant women ; Preservation ; Ribonucleic acid ; Risk factors ; RNA ; RNA, Viral - metabolism ; Staining ; Studies ; Swine ; Thymus ; Tissues ; Uterus ; Uterus - metabolism ; Uterus - virology ; Vasculitis ; Veterinary colleges ; Viruses</subject><ispartof>PloS one, 2017-03, Vol.12 (3), p.e0173360-e0173360</ispartof><rights>COPYRIGHT 2017 Public Library of Science</rights><rights>2017 Novakovic et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. 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The objectives of this study were to evaluate distribution and degree of apoptosis in the uterine and fetal placental tissues during the experimental type 2 PRRS virus (PRRSV) infection and determine associations between apoptosis at the MFI, PRRSV RNA concentration and antigen staining intensity, PRRSV-induced microscopic lesions, and fetal preservation status. A total of 114 naïve, high-health pregnant gilts were inoculated with type 2 PRRSV on gestation day 85±1 with euthanasia 21 days later; 19 sham-inoculated gilts served as controls. Two hundred and fifty samples of uterine tissue with fetal placenta were selected based on negative, low PRRSV RNA, and high PRRSV RNA concentration (0, < or > 2.7 log10 copies/mg, respectively). TUNEL assay was used to detect apoptosis in the endometrium and at the MFI. PRRSV RNA concentration and numbers of PRRSV immunopositive cells in uterine and placental tissue were positively associated with the severity of apoptosis in the endometrium and the MFI (P<0.001, P<0.05 and P<0.001, respectively). The number of TUNEL positive cells at the MFI was also positively associated with the severity (P<0.001) of vasculitis, but not total numbers of inflammatory cells in the endometrium. Increased numbers of TUNEL positive cells at the MFI were associated with PRRSV load in the fetal thymus, and greater odds of meconium staining of the fetus at 21 days post infection (P<0.001 for both). These findings suggest an important role of apoptosis in the pathogenesis of uterine epithelial and trophoblastic cell death at the MFI. Moreover, apoptosis at the MFI is significantly associated with fetal demise during in utero type 2 PRRSV infection.]]></description><subject>Analysis</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Biology and Life Sciences</subject><subject>Cell death</subject><subject>Endometrium</subject><subject>Euthanasia</subject><subject>Female</subject><subject>Fetuses</subject><subject>Genetic aspects</subject><subject>Gestation</subject><subject>Health aspects</subject><subject>In Situ Nick-End Labeling</subject><subject>Infections</subject><subject>Inflammation</subject><subject>Lesions</subject><subject>Maternal-Fetal Exchange</subject><subject>Meconium</subject><subject>Medicine and Health Sciences</subject><subject>Pathogenesis</subject><subject>Pathology</subject><subject>Placenta</subject><subject>Placenta - metabolism</subject><subject>Placenta - virology</subject><subject>Porcine reproductive and respiratory syndrome</subject><subject>Porcine Reproductive and Respiratory Syndrome - pathology</subject><subject>Porcine respiratory and reproductive syndrome virus</subject><subject>Porcine respiratory and reproductive syndrome virus - genetics</subject><subject>Porcine respiratory and reproductive syndrome virus - pathogenicity</subject><subject>Pregnancy</subject><subject>Pregnant women</subject><subject>Preservation</subject><subject>Ribonucleic acid</subject><subject>Risk factors</subject><subject>RNA</subject><subject>RNA, Viral - metabolism</subject><subject>Staining</subject><subject>Studies</subject><subject>Swine</subject><subject>Thymus</subject><subject>Tissues</subject><subject>Uterus</subject><subject>Uterus - metabolism</subject><subject>Uterus - virology</subject><subject>Vasculitis</subject><subject>Veterinary 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2 porcine reproductive and respiratory syndrome virus infection increases apoptosis at the maternal-fetal interface in late gestation pregnant gilts</title><author>Novakovic, Predrag ; Harding, John C S ; Al-Dissi, Ahmad N ; Detmer, Susan E</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c725t-6b40d180ba43f52b6a646bec6ca7802086f9c7b9019efcd270471f527cc1bc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Analysis</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Biology and Life Sciences</topic><topic>Cell death</topic><topic>Endometrium</topic><topic>Euthanasia</topic><topic>Female</topic><topic>Fetuses</topic><topic>Genetic aspects</topic><topic>Gestation</topic><topic>Health aspects</topic><topic>In Situ Nick-End Labeling</topic><topic>Infections</topic><topic>Inflammation</topic><topic>Lesions</topic><topic>Maternal-Fetal 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Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Novakovic, Predrag</au><au>Harding, John C S</au><au>Al-Dissi, Ahmad N</au><au>Detmer, Susan E</au><au>Kanellopoulos-Langevin, Colette</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Type 2 porcine reproductive and respiratory syndrome virus infection increases apoptosis at the maternal-fetal interface in late gestation pregnant gilts</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2017-03-02</date><risdate>2017</risdate><volume>12</volume><issue>3</issue><spage>e0173360</spage><epage>e0173360</epage><pages>e0173360-e0173360</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract><![CDATA[The pathogenesis of fetal death associated with porcine reproductive and respiratory syndrome (PRRS) is hypothesized to be a consequence of PRRS virus-induced apoptosis at the maternal-fetal interface (MFI). The objectives of this study were to evaluate distribution and degree of apoptosis in the uterine and fetal placental tissues during the experimental type 2 PRRS virus (PRRSV) infection and determine associations between apoptosis at the MFI, PRRSV RNA concentration and antigen staining intensity, PRRSV-induced microscopic lesions, and fetal preservation status. A total of 114 naïve, high-health pregnant gilts were inoculated with type 2 PRRSV on gestation day 85±1 with euthanasia 21 days later; 19 sham-inoculated gilts served as controls. Two hundred and fifty samples of uterine tissue with fetal placenta were selected based on negative, low PRRSV RNA, and high PRRSV RNA concentration (0, < or > 2.7 log10 copies/mg, respectively). TUNEL assay was used to detect apoptosis in the endometrium and at the MFI. PRRSV RNA concentration and numbers of PRRSV immunopositive cells in uterine and placental tissue were positively associated with the severity of apoptosis in the endometrium and the MFI (P<0.001, P<0.05 and P<0.001, respectively). The number of TUNEL positive cells at the MFI was also positively associated with the severity (P<0.001) of vasculitis, but not total numbers of inflammatory cells in the endometrium. Increased numbers of TUNEL positive cells at the MFI were associated with PRRSV load in the fetal thymus, and greater odds of meconium staining of the fetus at 21 days post infection (P<0.001 for both). These findings suggest an important role of apoptosis in the pathogenesis of uterine epithelial and trophoblastic cell death at the MFI. Moreover, apoptosis at the MFI is significantly associated with fetal demise during in utero type 2 PRRSV infection.]]></abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>28253336</pmid><doi>10.1371/journal.pone.0173360</doi><tpages>e0173360</tpages><orcidid>https://orcid.org/0000-0003-3488-277X</orcidid><oa>free_for_read</oa></addata></record> |
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source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Public Library of Science (PLoS) Journals Open Access; PubMed Central; Free Full-Text Journals in Chemistry |
subjects | Analysis Animals Apoptosis Biology and Life Sciences Cell death Endometrium Euthanasia Female Fetuses Genetic aspects Gestation Health aspects In Situ Nick-End Labeling Infections Inflammation Lesions Maternal-Fetal Exchange Meconium Medicine and Health Sciences Pathogenesis Pathology Placenta Placenta - metabolism Placenta - virology Porcine reproductive and respiratory syndrome Porcine Reproductive and Respiratory Syndrome - pathology Porcine respiratory and reproductive syndrome virus Porcine respiratory and reproductive syndrome virus - genetics Porcine respiratory and reproductive syndrome virus - pathogenicity Pregnancy Pregnant women Preservation Ribonucleic acid Risk factors RNA RNA, Viral - metabolism Staining Studies Swine Thymus Tissues Uterus Uterus - metabolism Uterus - virology Vasculitis Veterinary colleges Viruses |
title | Type 2 porcine reproductive and respiratory syndrome virus infection increases apoptosis at the maternal-fetal interface in late gestation pregnant gilts |
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