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  • 1
    Language: English
    In: PloS one, 2017, Vol.12 (3), p.e0173360-e0173360
    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〈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.
    Subject(s): 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 ; Research ; Ribonucleic acid ; Risk factors ; RNA ; RNA, Viral - metabolism ; Staining ; Studies ; Swine ; Thymus ; Tissues ; Uterus ; Uterus - metabolism ; Uterus - virology ; Vasculitis ; Veterinary colleges ; Viruses
    ISSN: 1932-6203
    E-ISSN: 1932-6203
    Source: Academic Search Ultimate
    Source: PubMed Central
    Source: DOAJ Directory of Open Access Journals - Not for CDI Discovery
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  • 2
    Language: English
    In: Frontiers in genetics, 2019-01-08, Vol.9, p.660-660
    Description: The objective of this study was to extract novel phenotypes related to disease resilience using daily feed intake data from growing pigs under a multifactorial natural disease challenge that was designed to mimic a commercial environment with high disease pressure to maximize expression of resilience. Data used were the first 1,341 crossbred wean-to-finish pigs from a research facility in Quebec, Canada. The natural challenge was established under careful veterinary oversight by seeding the facility with diseased pigs from local health-challenged farms, targeting various viral and bacterial diseases, and maintaining disease pressure by entering batches of 60-75 pigs in a continuous flow system. Feed intake (FI) is sensitive to disease, as pigs tend to eat less when they become ill. Four phenotypes were extracted from the individual daily FI data during finishing as novel measures of resilience. The first two were daily variability in FI or FI duration, quantified by the root mean square error (RMSE) from the within individual regressions of FI or duration at the feeder (DUR) on age (RMSEFI and RMSEDUR). The other two were the proportion of off-feed days, classified based on negative residuals from a 5% quantile regression (OR) of daily feed intake or duration data on age across all pigs (QR(FI) and QR(DUR)). Mortality and treatment rate had a heritability of 0.13 (+/- 0.05) and 0.29 (+/- 0.07), respectively. Heritability estimates for RMSEFI, RMSEDUR, QR(FI), and QR(DuR) were 0.21 (+/- 0.07) 0.26 (+/- 0.07), 0.15 (+/- 0.06), and 0.23 (+/- 0.07), respectively. Genetic correlations of RMSE and QR measures with mortality and treatment rate ranged from 0.37 to 0.85, with QR measures having stronger correlations with both. Estimates of genetic correlations of RMSE measures with production traits were typically low, but often favorable (e.g., -0.31 between RMSEFI and finishing ADG). Although disease resilience was our target, fluctuations in FI and duration can be caused by many factors other than disease and should be viewed as overall indicators of general resilience to a variety of stressors. In conclusion, daily variation in FI or duration at the feeder can be used as heritable measures of resilience.
    Subject(s): Analysis ; Animal feeding and feeds ; Bacterial infections ; disease resistance ; feed intake ; feeding duration ; Food and nutrition ; Genetics ; Genetics & Heredity ; Growth ; Life Sciences & Biomedicine ; Phenotype ; pigs ; Research ; resilience ; Science & Technology ; Swine
    ISSN: 1664-8021
    E-ISSN: 1664-8021
    Source: Web of Science - Science Citation Index Expanded - 2019〈img src="http://exlibris-pub.s3.amazonaws.com/fromwos-v2.jpg" /〉
    Source: PubMed Central
    Source: DOAJ Directory of Open Access Journals - Not for CDI Discovery
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  • 3
    Language: English
    In: PloS one, 2014, Vol.9 (8), p.e106399-e106399
    Description: "Brachyspira hampsonii" causes disease indistinguishable from swine dysentery, and the structure of the intestinal microbiome likely plays a role in determining susceptibility of individual pigs to infection and development of clinical disease. The objectives of the current study were to determine if the pre-inoculation fecal microbiota differed between inoculated pigs that did (INOC MH) or did not (INOC non-MH) develop mucohaemorrhagic diarrhea following challenge with "B. hampsonii", and to quantify changes in the structure of the microbiome following development of clinical disease. Fecal microbiota profiles were generated based on amplification and sequencing of the cpn60 universal target sequence from 89 samples from 18 pigs collected at -8, -5, -3 and 0 days post-inoculation, and at termination. No significant differences in richness, diversity or taxonomic composition distinguished the pre-inoculation microbiomes of INOC MH and INOC non-MH pigs. However, the development of bloody diarrhea in inoculated pigs was associated with perturbation of the microbiota relative to INOC non-MH or sham-inoculated control pigs. Specifically, the fecal microbiota of INOC MH pigs was less dense (fewer total 16S rRNA copies per gram of feces), and had a lower Bacteroidetes:Firmicutes ratio. Further investigation of the potential long-term effects of Brachyspira disease on intestinal health and performance is warranted.
    Subject(s): Animals ; Biology and Life Sciences ; Brachyspira - physiology ; Chemical properties ; Deoxyribonucleic acid ; Development and progression ; Diarrhea ; Diarrhea - microbiology ; Diarrhea - veterinary ; Disease ; DNA ; DNA, Bacterial - analysis ; Dysentery ; Fecal microflora ; Feces ; Feces - microbiology ; Gastrointestinal Hemorrhage - microbiology ; Gastrointestinal Hemorrhage - veterinary ; Genomes ; Gram-Negative Bacterial Infections - microbiology ; Gram-Negative Bacterial Infections - veterinary ; Gram-Positive Bacteria - classification ; Gram-Positive Bacteria - isolation & purification ; Infections ; Inoculation ; Intestine ; Laboratories ; Livestock ; Long-term effects ; Microbiology ; Microbiomes ; Microbiota ; Microbiota (Symbiotic organisms) ; RNA ; rRNA 16S ; Studies ; Swine ; Swine Diseases - microbiology ; Swine dysentery ; Veterinary colleges ; Veterinary medicine ; Waterborne diseases
    ISSN: 1932-6203
    E-ISSN: 1932-6203
    Source: Academic Search Ultimate
    Source: PubMed Central
    Source: DOAJ Directory of Open Access Journals - Not for CDI Discovery
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  • 4
    Language: English
    In: PloS one, 2014, Vol.9 (10), p.e109541-e109541
    Description: The severity of porcine reproductive and respiratory syndrome was compared in pregnant gilts originating from high and low birth weight litters. One-hundred and eleven pregnant gilts experimentally infected with porcine reproductive and respiratory syndrome virus on gestation day 85 (±1) were necropsied along with their fetuses 21 days later. Ovulation rates and litter size did not differ between groups, but fetuses from low birth weight gilts were shorter, lighter and demonstrated evidence of asymmetric growth with large brain:organ weight ratios (i.e. brain sparing). The number of intrauterine growth retarded fetuses, defined by brain:organ weight ratios greater than 1 standard deviation from the mean, was significantly greater in low, compared to high, birth weight gilts. Although γδ T cells significantly decreased over time in high compared to low birth weight gilts, viral load in serum and tissues, gilt serum cytokine levels, and litter outcome, including the percent dead fetuses per litter, did not differ by birth weight group. Thus, this study provided no substantive evidence that the severity of porcine reproductive and respiratory syndrome is affected by dam birth weight. However, intrauterine growth retarded fetuses had lower viral loads in both fetal thymus and in endometrium adjacent to the umbilical stump. Crown rump length did not significantly differ between fetuses that survived and those that died at least one week prior to termination. Taken together, this study clearly demonstrates that birth weight is a transgenerational trait in pigs, and provides evidence that larger fetuses are more susceptible to transplacental PRRSv infection.
    Subject(s): Animals ; B cells ; Biology and Life Sciences ; Birth Weight ; Brain ; Childbirth & labor ; Comparative analysis ; Endometrium ; Epigenetics ; Female ; Fetal Growth Retardation - pathology ; Fetal Growth Retardation - veterinary ; Fetal Growth Retardation - virology ; Fetus - virology ; Fetuses ; Gestation ; Growth ; Growth rate ; Hogs ; Litter ; Low-birth-weight ; Lymphocytes ; Lymphocytes T ; Mortality ; Organ weight ; Ovulation ; Porcine reproductive and respiratory syndrome ; Porcine Reproductive and Respiratory Syndrome - pathology ; Porcine Reproductive and Respiratory Syndrome - virology ; Porcine respiratory and reproductive syndrome virus - isolation & purification ; Pregnancy ; Pregnancy Complications, Infectious - pathology ; Pregnancy Complications, Infectious - veterinary ; Pregnancy Complications, Infectious - virology ; Pregnant women ; Risk factors ; Swine ; Swine - virology ; T cells ; Thymus ; Tissues ; Veterinary colleges ; Viruses ; Weight reduction
    ISSN: 1932-6203
    E-ISSN: 1932-6203
    Source: Academic Search Ultimate
    Source: PubMed Central
    Source: DOAJ Directory of Open Access Journals - Not for CDI Discovery
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  • 5
    Language: English
    In: PloS one, 2013, Vol.8 (2), p.e57146-e57146
    Description: Mucohaemorrhagic diarrhea caused by Brachyspira hyodysenteriae, swine dysentery, is a severe production limiting disease of swine. Recently, pigs in western Canada with clinical signs indistinguishable from swine dysentery were observed. Despite the presence of spirochetes on fecal smears, recognized Brachyspira spp. including B. hyodysenteriae could not be identified. A phylogenetically distinct Brachyspira, called "B. hampsonii" strain 30446, however was isolated. The purpose of this study was to experimentally reproduce mucohaemorrhagic colitis and characterize strain 30446 shedding following inoculation. Eighteen 13-week-old pigs were randomly assigned to inoculation (n = 12) or control (n = 6) groups in each of two trials. In trial 1, pigs were inoculated with a tissue homogenate collected from clinically affected field cases. In trial 2, pigs were inoculated with a pure broth culture of strain 30446. In both trials, mucohaemorrhagic diarrhea was significantly more common in inoculated pigs than controls, all of which remained healthy. In animals with mucohaemorrhagic diarrhea, significantly more spirochetes were observed on Gram stained fecal smears, and higher numbers of strain 30446 genome equivalents were detected by quantitative PCR (qPCR). Strain 30446 was cultured from colon and/or feces of all affected but no control animals at necropsy. "Brachyspira hampsonii" strain 30446 causes mucohaemorrhagic diarrhea in pigs following a 4-9 day incubation period. Fecal shedding was detectable by day 4 post inoculation, and rarely preceded the onset of mucoid or haemorrhagic diarrhea by more than 2 days. Culture and 30446-specific qPCR are reliable methods of detection of this organism in feces and tissues of diarrheic pigs. The emergence of a novel Brachyspira spp., such as "B. hampsonii", creates diagnostic challenges including higher risk of false negative diagnostic tests. We therefore recommend diagnostic laboratories routinely use Brachyspira culture, nox-based and species-specific PCR, and DNA sequencing to diagnose Brachyspira-associated colitis in pigs.
    Subject(s): Animal Husbandry ; Animals ; Biology ; Brachyspira - physiology ; Clinical trials ; Colitis ; Colitis - diagnosis ; Colitis - microbiology ; Colitis - pathology ; Colon ; Colon - microbiology ; Colon - pathology ; Culture ; Deoxyribonucleic acid ; Diagnostic systems ; Diarrhea ; Diarrhea - diagnosis ; Diarrhea - microbiology ; Diarrhea - pathology ; Disease control ; DNA ; DNA sequencing ; Dysentery ; Feces ; Feces - microbiology ; Gangrene ; Gastrointestinal Hemorrhage - diagnosis ; Gastrointestinal Hemorrhage - microbiology ; Gastrointestinal Hemorrhage - pathology ; Gene sequencing ; Genomes ; Genomics ; Gram-Negative Bacterial Infections - diagnosis ; Gram-Negative Bacterial Infections - microbiology ; Gram-Negative Bacterial Infections - pathology ; Hogs ; Incubation ; Infections ; Inflammatory bowel disease ; Inoculation ; Livestock ; Medicine ; Mucus - metabolism ; Nucleotide sequencing ; Phylogeny ; Polymerase chain reaction ; Shedding ; Spirochetes ; Swine ; Swine - microbiology ; Swine Diseases - diagnosis ; Swine Diseases - microbiology ; Swine Diseases - pathology ; Swine dysentery ; Tissues ; Veterinary colleges ; Veterinary medicine ; Veterinary Science ; Waterborne diseases
    ISSN: 1932-6203
    E-ISSN: 1932-6203
    Source: Academic Search Ultimate
    Source: PubMed Central
    Source: DOAJ Directory of Open Access Journals - Not for CDI Discovery
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  • 6
    Language: English
    In: PloS one, 2016, Vol.11 (3), p.e0151198-e0151198
    Description: The pathogenesis of fetal death caused by porcine reproductive and respiratory syndrome virus (PRRSV) remains unclear. The objective of this study was to improve our understanding of the pathogenesis by assessing potential relationships between specific histopathological lesions and PRRSV RNA concentration in the fetuses and the maternal-fetal interface. Pregnant gilts were inoculated with PRRSV (n = 114) or sham inoculated (n = 19) at 85±1 days of gestation. Dams and their litters were humanely euthanized and necropsied 21 days later. PRRSV RNA concentration was measured by qRT-PCR in the maternal-fetal interface and fetal thymus (n = 1391). Presence of fetal lesions was positively related to PRRSV RNA concentration in the maternal-fetal interface and fetal thymus (P〈0.05 for both), but not to the distribution or severity of vasculitis, or the severity of endometrial inflammation. The presence of fetal and umbilical lesions was associated with greater odds of meconium staining (P〈0.05 for both). The distribution and severity of vasculitis in endometrium were not significantly related to PRRSV RNA concentration in maternal-fetal interface or fetal thymus. Endometrial inflammation severity was positively related to distribution and severity of vasculitis in endometrium (P〈0.001 for both). Conclusions from this study suggest that type 2 PRRSV infection in pregnant gilts induces significant histopathological lesions at maternal-fetal interface, but they are not associated with presence of PRRSV in the maternal-fetal interface at 21 days post infection. Conversely, fetal pathological lesions are associated with presence of PRRSV in the maternal-fetal interface and fetal thymus, and meconium staining is significantly associated with the presence of both fetal and umbilical lesions observed 21 days post infection.
    Subject(s): Animals ; Biology and Life Sciences ; Development and progression ; Disease ; Diseases ; Drug dosages ; Endometriosis - metabolism ; Endometriosis - pathology ; Endometriosis - virology ; Endometrium ; Female ; Fetus - embryology ; Fetus - pathology ; Fetus - virology ; Fetuses ; Genetic aspects ; Genotype ; Gestation ; Hogs ; Identification and classification ; Infections ; Lesions ; Meconium ; Medicine and Health Sciences ; Mutation ; Pathogenesis ; Pathology ; Placenta - metabolism ; Placenta - pathology ; Placenta - virology ; Porcine Reproductive and Respiratory Syndrome - metabolism ; Porcine Reproductive and Respiratory Syndrome - pathology ; Porcine respiratory and reproductive syndrome virus - metabolism ; Pregnancy ; Pregnancy Complications, Infectious - metabolism ; Pregnancy Complications, Infectious - pathology ; Pregnancy Complications, Infectious - virology ; Ribonucleic acid ; RNA ; RNA virus infections ; RNA, Viral - metabolism ; Staining ; Swine ; Swine - metabolism ; Swine - virology ; Thymus ; Thymus Gland - embryology ; Thymus Gland - pathology ; Thymus Gland - virology ; Umbilical cord ; Vasculitis ; Vasculitis - metabolism ; Vasculitis - pathology ; Vasculitis - virology ; Veterinary colleges ; Veterinary medicine ; Virulence (Microbiology) ; Viruses
    ISSN: 1932-6203
    E-ISSN: 1932-6203
    Source: Academic Search Ultimate
    Source: PubMed Central
    Source: DOAJ Directory of Open Access Journals - Not for CDI Discovery
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  • 7
    Language: English
    In: Veterinary research (Paris), 2020-03-30, Vol.51 (1), p.47-47
    Description: To better understand the host response to porcine reproductive and respiratory virus-2 (PRRSV2) we evaluated circulating thyroid hormone and associated gene expression in a late gestation challenge model. Pregnant gilts were inoculated at gestation day 85 and fetal samples collected at either 12 or 21 days post-infection (dpi). A subset of fetuses was selected for analysis based on viability and viral load categorized as either uninfected-viable (UNIF), high viral load viable (HV-VIA) or high viral load meconium stained (HV-MEC) and were compared with gestational age matched controls (CON). In dams, circulating levels of total T3 and T4 decreased in the acute period following infection and rebounded by 21 dpi. A similar effect was observed in fetuses, but was largely restricted to HV-VIA and HV-MEC, with minimal decrease noted in UNIF relative to CON at 21 dpi. Gene expression in fetal heart at 12 dpi showed significant decompensatory transcription of thyroid hormone transporters (SLC16A2) and deiodinases (DIO2, DIO3), which was not observed in brain. Correspondingly, genes associated with cell cycle progression (CDK1,2,4) were downregulated in only the heart of highly infected fetuses, while expression of their inhibitor (CDKN1A) was upregulated in both tissues. Finally, expression of genes associated with cardiac stress including CAMKD and AGT were upregulated in the hearts of highly infected fetuses, and a shift in expression of MYH6 to MYH7 was observed in HV-MEC fetuses specifically. Collectively, the results suggest PRRSV2 infection causes a hypothyroid state that disproportionally impacts the fetal heart over the brain.
    Subject(s): Brain research ; Experiments ; Fetuses ; Gene expression ; Heart ; Hormones ; Infections ; Life Sciences ; Placenta ; Thyroid gland
    ISSN: 1297-9716
    ISSN: 0928-4249
    E-ISSN: 1297-9716
    Source: BioMedCentral Open Access
    Source: PubMed Central
    Source: DOAJ Directory of Open Access Journals - Not for CDI Discovery
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  • 8
    Language: English
    In: PloS one, 2014, Vol.9 (4), p.e96104-e96104
    Description: In spite of extensive research, the mechanisms of reproductive disease associated with Porcine Reproductive and Respiratory Syndrome virus (PRRSv) are still poorly understood. The objectives of this large scale study were to evaluate associations between viral load and fetal preservation, determine the impact of type 2 PRRSv on fetal weights, and investigate changes in ORF5 PRRSv genome in dams and fetuses during a 21-day period following challenge. At gestation day 85 (±1), 114 gilts were experimentally infected with type 2 PRRSv, while 19 gilts served as reference controls. At necropsy, fetuses were categorized according to their preservation status and tissue samples were collected. PRRSv RNA concentrations were measured in gilt serum collected on days 0, 2, 6, and 21 post-infection, as well as in gilt and fetal tissues collected at termination. Fetal mortality was 41±22.8% in PRRS infected litters. Dead fetuses appeared to cluster in some litters but appeared solitary or random in others. Nine percent of surviving piglets were meconium-stained. PRRSv RNA concentration in fetal thymus, fetal serum and endometrium differed significantly across preservation category and was greatest in tissues of meconium-stained fetuses. This, together with the virtual absence of meconium staining in non-infected litters indicates it is an early pathological condition of reproductive PRRS. Viral load in fetal thymus and in fetal serum was positively associated with viral load in endometrium, suggesting the virus exploits dynamic linkages between individual maternal-fetal compartments. Point mutations in ORF5 sequences from gilts and fetuses were randomly located in 20 positions in ORF5, but neither nucleotide nor amino acid substitutions were associated with fetal preservation. PRRSv infection decreased the weights of viable fetuses by approximately 17%. The considerable variation in gilt and fetal outcomes provides tremendous opportunity for more detailed investigations of potential mechanisms and single nucleotide polymorphisms associated with fetal death.
    Subject(s): Abortion, Veterinary - virology ; Amino acids ; Analysis ; Animals ; Biology and life sciences ; Care and treatment ; Compartments ; Diagnosis ; Endometrium ; Endometrium - virology ; Female ; Fetal Weight ; Fetuses ; Genetic aspects ; Genetic Association Studies ; Genetic polymorphisms ; Genomes ; Genotype ; Gestation ; Gestational Age ; Hogs ; Infections ; Linkages ; Meconium ; Medicine and Health Sciences ; Mutation ; Phenotype ; Physiological aspects ; Polymorphism, Single Nucleotide ; Porcine reproductive and respiratory syndrome ; Porcine Reproductive and Respiratory Syndrome - mortality ; Porcine Reproductive and Respiratory Syndrome - virology ; Porcine respiratory and reproductive syndrome virus - genetics ; Pregnancy ; Preservation ; Ribonucleic acid ; Risk factors ; RNA ; RNA, Viral - genetics ; Sequence Analysis, DNA ; Single-nucleotide polymorphism ; Sus scrofa ; Swine ; Thymus ; Thymus Gland - virology ; Tissues ; Veterinary colleges ; Viral Envelope Proteins - genetics ; Viral Load ; Viruses ; Weaning
    ISSN: 1932-6203
    E-ISSN: 1932-6203
    Source: Academic Search Ultimate
    Source: PubMed Central
    Source: DOAJ Directory of Open Access Journals - Not for CDI Discovery
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  • 9
    Language: English
    In: PloS one, 2020-04-27, Vol.15 (4), p.e0231942-e0231942
    Description: Salmonella enterica serovar Typhimurium is an animal welfare and public health concern due to its ability to parasite livestock and potentially contaminate pork products. To reduce Salmonella shedding and the risk of pork contamination, antibiotic therapy is used and can contribute to antimicrobial resistance. Here we hypothesized that immune system education by the microbiota can play a role in intestinal resilience to infection. We used amoxicillin (15mg/Kg) to modulate the intestinal microbiome of 10 piglets, paired with same age pigs that received a placebo (n = 10) from 0 to 14 days of age. Animals were euthanized at 4-weeks old. Each pig donated colon sections for ex vivo culture (n = 20 explants/pig). Explants were inoculated with S . Typhimurium, PBS or LPS (n = 6 explants/pig/group, plus technical controls). The gut bacteriome was characterized by sequencing of the 16S rRNA at 7, 21 days of age, and upon in vitro culture. Explants response to infection was profiled through high-throughput mRNA sequencing. In vivo antibiotic treatment led to β-diversity differences between groups at all times ( P 〈0.05), while α-diversity did not differ between amoxicillin and placebo groups on day 21 and at euthanasia ( P 〈0.03 on day 7). Explant microbiomes were not different from in vivo . In vitro challenge with S . Typhimurium led to lower necrosis scores in explants from amoxicillin-treated pigs, when compared to explants placebo-treated pigs ( P 〈0.05). This was coupled with the activation of immune-related pathways in explants from amoxicillin-treated pigs (IL-2 production, NO production, BCR activation), when compared to placebo-treated pigs. In addition, several DNA repair and intestinal wound healing pathways were also only activated in explants from amoxicillin-treated pigs. Taken together, these findings suggest that immune education by the amoxicillin-disturbed microbiota may have contributed to mitigate intestinal lesions following pathogen exposure.
    Subject(s): Activation ; Age ; Amoxicillin ; Animal welfare ; Antibiotics ; Antimicrobial agents ; Antimicrobial resistance ; Biology and Life Sciences ; Biotechnology industry ; Colon ; Contamination ; Deoxyribonucleic acid ; DNA ; DNA repair ; Drug dosages ; Drug resistance in microorganisms ; E coli ; Education ; Epigenetic inheritance ; Euthanasia ; Explants ; Gene sequencing ; Health aspects ; Hogs ; Husbandry ; Immune system ; Infections ; Interleukin 2 ; International economic relations ; Intestine ; Lipopolysaccharides ; Livestock ; Medicine and Health Sciences ; Microbiomes ; Microbiota ; Microbiota (Symbiotic organisms) ; mRNA ; Necrosis ; Parasites ; Pathogens ; Pathways ; Pork ; Pork industry ; Public health ; RNA ; RNA sequencing ; rRNA 16S ; Salmonella ; Swine ; Veterinary colleges ; Veterinary medicine ; Wound healing
    ISSN: 1932-6203
    E-ISSN: 1932-6203
    Source: Academic Search Ultimate
    Source: PubMed Central
    Source: DOAJ Directory of Open Access Journals - Not for CDI Discovery
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  • 10
    Language: English
    In: BMC genomics, 2016-05-20, Vol.17 (370), p.383-383
    Description: Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) infection of pregnant pigs can result in congenital infection and ultimately fetal death. Little is known about immune responses to infection at the maternal-fetal interface and in the fetus itself, or the molecular events behind virus transmission and disease progression in the fetus. To investigate these processes, RNA-sequencing of two sites, uterine endothelium with adherent placental tissue and fetal thymus, was performed 21 days post-challenge on four groups of fetuses selected from a large PRRSV challenge experiment of pregnant gilts: control (CON), uninfected (UNINF), infected (INF), and meconium-stained (MEC) (n = 12/group). Transcriptional analyses consisted of multiple contrasts between groups using two approaches: differential gene expression analysis and weighted gene co-expression network analysis (WGCNA). Biological functions, pathways, and regulators enriched for differentially expressed genes or module members were identified through functional annotation analyses. Expression data were validated by reverse transcription quantitative polymerase chain reaction (RTqPCR) carried out for 16 genes of interest. The immune response to infection in endometrium was mainly adaptive in nature, with the most upregulated genes functioning in either humoral or cell-mediated immunity. In contrast, the expression profile of infected fetal thymus revealed a predominantly innate immune response to infection, featuring the upregulation of genes regulated by type I interferon and pro-inflammatory cytokines. Fetal infection was associated with an increase in viral load coupled with a reduction in T cell signaling in the endometrium that could be due to PRRSV-controlled apoptosis of uninfected bystander cells. There was also evidence for a reduction in TWIST1 activity, a transcription factor involved in placental implantation and maturation, which could facilitate virus transmission or fetal pathology through dysregulation of placental function. Finally, results suggested that events within the fetus could also drive fetal pathology. Thymus samples of meconium-stained fetuses exhibited an increase in the expression of pro-inflammatory cytokine and granulocyte genes previously implicated in swine infectious disease pathology. This study identified major differences in the response to PRRSV infection in the uterine endometrium and fetus at the gene expression level, and provides insight into the molecular basis of virus transmission and disease progression.
    Subject(s): Animals ; Biological response modifiers ; Cluster Analysis ; Development and progression ; Disease transmission ; Endometrium - metabolism ; Female ; Fetal death ; Fetus ; Fetus - metabolism ; Gene ; Gene Expression Profiling ; Gene Expression Regulation ; Genome-Wide Association Study ; Host-Pathogen Interactions - genetics ; Immune response ; Organ Specificity - genetics ; Pig ; Placenta - metabolism ; Porcine reproductive and respiratory syndrome ; Porcine Reproductive and Respiratory Syndrome - genetics ; Porcine Reproductive and Respiratory Syndrome - virology ; Porcine respiratory and reproductive syndrome virus ; Pregnancy ; PRRSV ; Reproducibility of Results ; Research ; RNA-sequencing ; Signal Transduction ; Swine ; Transcriptome ; Viral Load
    ISSN: 1471-2164
    E-ISSN: 1471-2164
    Source: BioMedCentral Open Access
    Source: Academic Search Ultimate
    Source: PubMed Central
    Source: DOAJ Directory of Open Access Journals - Not for CDI Discovery
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