Glaesserella parasuis serotype 4 HPS4-YC disrupts the integrity of the swine tracheal epithelial barrier and facilitates bacterial translocation.

Glaesserella parasuis (G. parasuis) is a commensal bacterium in the upper respiratory tract of pigs that can also cause the swine Glässer disease, which induces an intensive inflammatory response and results in significant economic losses to the swine industry worldwide. G. parasuis can cause disease through infection of the respiratory tract, resulting in systemic infection, but the mechanism is largely unknown. Recently we showed that Glaesserella parasuis serotype 4 (GPS4) increased swine tracheal epithelial barrier permeability, resulting in easier bacterial translocation. Tight junction proteins (TJ) play a crucial role in maintaining the integrity and impermeability of the epithelial barrier. GPS4 decreased the expression of the TJ ZO-1 and occludin in swine tracheal epithelial cells (STEC). Furthermore, the proinflammatory cytokines IL-6, IL-8 and TNF-α were significantly upregulated in GPS4-infected STEC, and both the MAPK and NF-κB signaling pathways were activated and contributed to the expression of TNF-α. We demonstrate that the production of proinflammatory cytokines, especially TNF-α, during GPS4 infection was involved in barrier dysfunction. Additionally, animal challenge experiments confirmed that GPS4 infection downregulated TJ in the lungs of piglets and induced a severe inflammatory response. In general, G. parasuis infection downregulated the expression of TJ and induced massive secretion of proinflammatory cytokines, resulting in epithelial barrier disruption and favoring bacterial infection. This study allowed us to better understand the mechanism by which G. parasuis crosses the respiratory tract of pigs.

Establishment of inflammatory model induced by Pseudorabies virus infection in mice.

BACKGROUND: Pseudorabies virus (PRV) infection leads to high mortality in swine. Despite extensive efforts, effective treatments against PRV infection are limited. Furthermore, the inflammatory response induced by PRV strain GXLB-2013 is unclear. OBJECTIVES: Our study aimed to investigate the inflammatory response induced by PRV strain GXLB-2013, establish an inflammation model to elucidate the pathogenesis of PRV infection further, and develop effective drugs against PRV infection. METHODS: Kunming mice were infected intramuscularly with medium, LPS, and different doses of PRV-GXLB-2013. Viral spread and histopathological damage to brain, spleen, and lung were determined at 7 days post-infection (dpi). Immune organ indices, levels of reactive oxygen species (ROS), nitric oxide (NO), and inflammatory cytokines, as well as levels of activity of COX-2 and iNOS were determined at 4, 7, and 14 dpi. RESULTS: At 105-106 TCID50 PRV produced obviously neurological symptoms and 100% mortality in mice. Viral antigens were detectable in kidney, heart, lung, liver, spleen, and brain. In addition, inflammatory injuries were apparent in brain, spleen, and lung of PRV-infected mice. Moreover, PRV induced increases in immune organ indices, ROS and NO levels, activity of COX-2 and iNOS, and the content of key pro-inflammatory cytokines, including interleukin (IL)-1ß, IL-6, tumor necrosis factor-α, interferon-γ and MCP-1. Among the tested doses, 10² TCID50 of PRV produced a significant inflammatory mediator increase. CONCLUSIONS: An inflammatory model induced by PRV infection was established in mice, and 10² TCID50 PRV was considered as the best concentration for the establishment of the model.

High pathogenicity island is associated with enhanced autophagy in pathogenic Escherichia coli HPI - infected macrophages.

High pathogenicity island (HPI), which is widely distributed in Escherichia coli (E. coli), can enhance the pathogenicity of E. coli. Thus the HPI positive E. coli could pose a threat to human and animal health. It remains to be elucidated how HPI affects the virulence of pathogenic E. coli. Autophagy is an important mechanism to maintain cellular homeostasis and an innate immunity responses of organisms against pathogens. The interaction between pathogenic E. coli possessing HPI (E. coli HPI) and host autophagy system has not been reported. In this study, it was demonstrated that pathogenic E. coli induced autophagy in 3D4/21 macrophages and HPI was associated with enhanced autophagy through transmission electron microscopy, immunofluorescence and real-time PCR. The PI3K/Akt/mTOR pathway is an important negative regulatory pathway for autophagy. Through detecting the expression of key genes of PI3K/Akt/mTOR pathway, it was speculated that HPI enhanced the inhibition of the signaling pathway stimulated by pathogenic E. coli. Furthermore, HPI inhibited the secretion of IFN-γ, while the presence of HPI did not significantly affect the secretion of IL-1ß. This work is the first attempt to explore the interplay between HPI carried by pathogenic E. coli and host cell autophagy. The findings might enable better understanding of the contribution of HPI to pathogenicity.

The role of somatostatin and its receptors (sstr2, sstr5) in the contractility of gilt inflamed uterus.

We studied the inflammation effect on somatostatin receptors subtypes 2 (sstr2) and 5 (sstr5) expression in myometrium and somatostatin influence alone or with sstr2 and sstr5 antagonists on the contractility of gilt inflamed uterus. On day 3 of the estrous cycle, either E.coli suspension (E.coli group) or saline (SAL group) were injected into uterine horns. In the control pigs (CON group), only laparotomy was performed. Eight days later, in the E.coli group developed severe acute endometritis. In this group, myometrial sstr2 mRNA expression lowered and protein expression increased compared to other groups. Compared to period before somatostatin administration, somatostatin did not change tension in myometrium and endometrium/myometrium of three groups, reduced amplitude and frequency in the CON and SAL groups, and increased amplitude and decreased frequency in the E.coli group. In this group, amplitude was increased by somatostatin compared to other groups. In the CON and SAL groups, sstr2 eliminated inhibitory somatostatin effect on amplitude, while sstr5 antagonist reversed inhibitory somatostatin effect on amplitude. In the E.coli group, sstr2 antagonist reversed stimulatory somatostatin effect on amplitude, while in sstr5 antagonist presence stimulatory somatostatin effect was more deepened compared to somatostatin action alone. After using sstr2 antagonist more deepened inhibitory somatostatin effect on frequency in the CON and E.coli groups was found. Sstr5 antagonist partly eliminated inhibitory somatostatin effect on frequency in the SAL group. Summarizing, the uterine inflammation increases the myometrial sstr2 protein expression; somatostatin raises amplitude of the inflamed uterus acting by sstr2, while drops this parameter by sstr5.

Participation of acetylcholine and its receptors in the contractility of inflamed porcine uterus.

This study analyzed the effect of inflammation on acetylcholine (ACh)-induced muscarinic receptors (MR)2 and MR3 conducted contractility of the porcine uterus. On Day 3 of the estrous cycle, either E.coli suspension (E.coli group) or saline (SAL group) was injected into uterine horns or laparotomy was performed (CON group). Eight days later, infected gilts developed severe acute endometritis. Compared to the period before ACh treatment, ACh (10-5 M) increased the tension in myometrium (MYO) and endometrium/myometrium (ENDO/MYO) of the CON group (P < 0.01) and in ENDO/MYO of the SAL group (P < 0.01), the amplitude in strips of the CON (P < 0.05) and SAL (MYO: P < 0.05, ENDO/MYO: P < 0.001) groups and the frequency in strips of the CON (MYO: P < 0.01, ENDO/MYO: P < 0.001) and SAL (P < 0.01) groups. In the E.coli group, ACh (10-5 M) reduced the amplitude in MYO (P < 0.05) and ENDO/MYO (P < 0.001), increased the frequency in MYO (P < 0.01) and ENDO/MYO (P < 0.001) and did not change (P > 0.05) the tension. ACh (10-5 M) in ENDO/MYO of the E.coli group, reduced the tension compared to the CON group (P < 0.05) and the amplitude compared to other groups (P < 0.001), while increased the frequency in relation to the SAL group (P < 0.05). MR2 antagonist (AF-DX 44 116) and ACh (10-5 M) reduced (by 16.92%, P < 0.01) the tension in MYO of the CON group and increased (P < 0.01) it in the E.coli group compared to the period before antagonist and ACh addition. In MYO of the SAL group, the tension was increased (P < 0.01) in response to MR3 antagonist (4-DAMP) and ACh (10-7, 10-6 M). In the E.coli group, these substances did not change (P > 0.05) the tension, but it was lower (P < 0.001) in MYO (ACh: 10-7 M) and ENDO/MYO (ACh: 10-5 M) than in the SAL group. MR2 or MR3 antagonists and ACh (10-5 M) increased (P < 0.05-0.001) the amplitude in strips of the CON and SAL groups and reduced it in the E.coli group (P < 0.001) compared to the period before antagonists and ACh use. This parameter in the E.coli group was lower (P < 0.001) after using MR2 or MR3 antagonists and ACh (10-6, 10-5 M) than in other groups. Both antagonists and ACh (10-5 M) reduced the frequency in the CON, SAL (P < 0.05) and E.coli (MR2 antagonist: P < 0.01, MR3 antagonist: P < 0.05) groups compared to period before antagonists and ACh addition. Data show that ACh reduces the contractility of the inflamed porcine uterus by MR2 and MR3, which suggests that pharmacological modulation of these receptors can be used to raise the contractility of an inflamed uterus.

Flaxseed oil supplementation improves intestinal function and immunity, associated with altered intestinal microbiome and fatty acid profile in pigs with intrauterine growth retardation.

Flaxseed oil (FO), enriched in n-3 polyunsaturated fatty acids (PUFAs), is an important oil source for intestinal development and health. We aimed to study the different effects of FO versus soybean oil (SO) on growth, intestinal health and immune function of neonates with intrauterine growth retardation (IUGR) using a weaned piglet model. Forty pairs of male IUGR and normal birth weight piglets, weaned at 21 ± 1 d, were fed diets containing either 4% FO or SO for 3 weeks consecutively. Growth performance, nutrient digestibility and intestinal function parameters, immunology and microbiota composition were determined. IUGR led to a poor growth rate, nutrient digestibility and abnormal immunology variables, whereas feeding FO diet improved systemic and gut immunity, as indicated by increased plasma concentration of immunoglobulin G and decreased CD3+CD8+ T lymphocytes, and down-regulated intestinal expression of genes (MyD88, NF-κB, TNF-α, IL-10). Although IUGR tended to decrease villous height, feeding FO diet tended to increase the villi-crypt ratio and up-regulated expressions of tight junction genes (Claudin-1 and ZO-1), together with increased mucosa contents of n-3 PUFAs and a lower Σn-6/Σn-3 ratio. Besides, FO diet decreased the abundance of pathogenic bacteria Spirochaetes, and increased phylum Actinobacteria, and genera Blautia and Bifidobacterium in colonic digesta. Our findings indicate that IUGR impairs growth rate, nutrient digestibility, and partly immunology variables, whereas feeding FO-supplemented diet could improve intestinal function and immunity of both IUGR and NBW pigs, associated with the altered gut microbiome and mucosal fatty acid profile.

Japanese Encephalitis Virus infection induces inflammation of swine testis through RIG-I-NF-ĸB signaling pathway.

Japanese Encephalitis Virus (JEV) is an important zoonotic flavivirus transmitted by mosquitos. JEV infection in sows primarily manifests as a reproductive disease such as abortion and transient infertility while in infected boars, it can cause orchitis. Previous studies mainly focused on the pathogenesis of human encephalitis caused by JEV infection, while few concentrations have been made to unveil the potential mechanism of reproductive dysfunction in JEV-infected pigs. In this study, histopathological analysis and immunohistochemistry staining was performed on testis of JEV-infected boars, indicating that JEV could infect testicular cells and cause inflammatory changes in testis. In vitro assays reveal that primary swine testicular cells and swine testis (ST) cells are highly permissive to JEV and significant inflammatory response was shown during JEV infection. Mechanically, we found that JEV infection increases the expression of retinoic acid-inducible gene I (RIG-I) and activates transcription factor NF-κB. Production of pro-inflammatory cytokines was greatly reduced in JEV infected testicular cells after knockout of RIG-I or treatment with the NF-κB specific inhibitor. In addition, activation of NF-κB was also significantly suppressed upon RIG-I knockout. Taken together, our results reveal that JEV could infect boar testicles, and RIG-I-NF-κB signaling pathway is involved in JEV-induced inflammation in swine testicular cells.

Relationship between haematological profile and progression or spontaneous regression of melanoma in the Melanoma-bearing Libechov Minipigs.

Haematological parameters, plasma iron concentration, and bodyweight were monitored in Melanoma-bearing Libechov Minipigs (MeLiM) from 5 to 18 weeks old. Animals with melanoma progression (P group) and spontaneous regression (SR group) were compared. The P group showed the lowest median values of red blood cell counts (RBC), haematocrit (HCT), haemoglobin concentration (HGB), and bodyweight, whereas the control white (tumour-free) pigs (C group) revealed the highest mean values of these parameters. The mean values of pigs with SR fell between the P and C groups. In addition, a stable concentration of plasma iron was found in the C group, while iron deficiency that increases with age was observed in the MeLiM groups. These results indicate that MeLiM are affected by cancer-related microcytic hypochromic anaemia. The lowest values of HGB, RBC, and HCT, together with the highest number of platelets (PLT) in the P group correspond to melanoma progression. Higher values of these parameters and lower PLT in the MeLiM pigs with SR reflected health improvement due to the destruction of melanoma cells during spontaneous regression. Monitoring of these haematological parameters can help distinguish MeLiM piglets with progression and spontaneous regression of melanoma in the early stages of postnatal development. The findings of this study correspond to findings in human patients in which cancer-related anaemia, thrombocytosis, and iron deficiency are often diagnosed.

Endometritis affects chemical coding of the dorsal root ganglia neurons supplying uterus in the sexually mature gilts.

This study reports on the influence of experimentally-induced uterine inflammation on chemical phenotypes, number and distribution of neurons in the dorsal root ganglia (DRGs) innervating the uterus in sexually mature gilts. On day 17 of the first studied estrous cycle, the uterine horns were injected with retrograde tracer Fast Blue (FB). After 28 days (on an expected day 3 of third studied estrous cycle), 50 ml of either saline (group SAL) or Escherichia coli (E. coli) suspension (109 colony-forming units/ml, group E. coli) were injected into each uterine horn. In the control pigs (group CON), only laparotomy was performed. Eight days later DRGs and uteri were collected. All infected gilts developed severe form of acute endometritis. By use of double immunofluorescence labelling the numbers of uterine perikarya expressing substance P (SP), calcitonin gene-related peptide (CGRP), neurokinin A (NKA), galanin (GAL) and pituitary adenylate cyclase-activating polypeptide (PACAP) were analyzed. Injection of E. coli decreased the total number of the FB positive perykaria in the Th10-S4 DRGs. We revealed an increase in the populations of uterine perikarya coded SP+/CGRP-, SP+/NKA-, SP-/NKA+, SP+/GAL+, SP+/GAL-, SP-/GAL+, SP+/PACAP+ and SP-/PACAP+. Our results suggest that uterine inflammation affects both the spatial and neurochemical organization pattern of uterine sensory innervation. Additionally, the inflammation may affect the transmission of sensory information from uterus to spinal cord.

I-FABP, Pig-MAP and TNF-α as biomarkers for monitoring gut-wall integrity in front of Salmonella Typhimurium and ETEC K88 infection in a weaned piglet model.

Having sensitive serum biomarkers able to determine the structural changes of the small intestine suffering from bacterial digestive diseases could be a valuable tool particularly in piglets at weaning, when intestinal infections are highly prevalent. We evaluated the usefulness of three inflammatory and gut-wall-integrity biomarkers to assess the degree of intestinal histo-morphological damage in piglets. Piglets were orally challenged with Salmonella Typhimurium or enterotoxigenic Escherichia coli (ETEC) to get a variable range of response according to individual variability. Forty-eight piglets were challenged with Salmonella Typhimurium and seventy-two with enterotoxigenic Escherichia coli K88. Clinical signs and faecal score were recorded. At Days 4 and 8 post-inoculation, blood was sampled, animals euthanised and distal ileum dissected. Morphological measures were obtained from the gut tissue, and serum tumour necrosis factor-alpha (TNF-α), pig major acute-phase protein (Pig-MAP) and intestinal fatty acid-binding protein (I-FABP) were determined. Animals developed mild-to-severe diarrhoea after the challenge. When analysing the complete set of analytical results, a high correlation was found among the three serum biomarkers. The most representative morphological indicator was the villus:crypt ratio (V:C), which showed a strong negative correlation with all three biomarkers. Regression analyses between faecal score and the previous variable showed linear relations. When the range of V:C was analysed, based on the quartile distribution of each serum variable, a marked increase in their concentration was observed with greater villus damage. Summarising, the combination of I-FABP, Pig-MAP and TNF-α may be useful for determining the intestinal injury degree and barrier integrity in recently weaned pigs.

Role of p53 in pseudorabies virus replication, pathogenicity, and host immune responses.

As a key cellular transcription factor that plays a central role in cellular responses to a broad range of stress factors, p53 has generally been considered as a host cell restriction factor for various viral infections. However, the defined roles of p53 in pseudorabies virus (PRV) replication, pathogenesis, and host responses remain unclear. In the present study, we initially constructed a p53 overexpressing a porcine kidney epithelial cell line (PK-15) to detect the effect of p53 on PRV replication in vitro. The results show that viral glycoprotein B (gB) gene copies and the titers of virus were significantly higher in p53 overexpressing PK-15 cells than in PK-15 and p53 inhibitor treated p53 overexpressing PK-15 cells. A similar result was also found in the p53 inhibitor PFT-α-treated PK-15 cells. We then examined the effects of p53 on PRV infection in vivo by using p53-knockout (p53-/-) mice. The results show that p53 knockout not only led to significantly reduced rates of mortality but also to reduced viral replication and development of viral encephalitis in the brains of mice following intracranial inoculation. Furthermore, we examined the effect of p53 knockout on the expression of the reported host cell regulators of PRV replication in the brains of mice by using RNA sequencing. The results show that p53 knockout downregulated the interferon (IFN) regulator genes, chemokine genes, and antiviral genes after PRV infection. This finding suggests that p53 positively regulates viral replication and pathogenesis both in vitro and in vivo. These findings offer novel targets of intrinsic host cell immunity for PRV infection.

A systematic literature mapping and meta-analysis of animal-based traits as indicators of production diseases in pigs.

The choice of animal-based traits to identify and deal with production diseases is often a challenge for pig farmers, researchers and other related professionals. This systematic review focused on production diseases, that is, the diseases that arise from management practices, affecting the digestive, locomotory and respiratory system of pigs. The aim was to classify all traits that have been measured and conduct a meta-analysis to quantify the impact of diseases on these traits so that these can be used as indicators for intervention. Data were extracted from 67 peer-reviewed publications selected from 2339 records. Traits were classified as productive (performance and carcass composition), behavioural, biochemical and molecular traits. A meta-analysis based on mixed models was performed on traits assessed more than five times across studies, using the package metafor of the R software. A total of 524 unique traits were recorded 1 to 31 times in a variety of sample material including blood, muscle, articular cartilage, bone or at the level of whole animal. No behavioural traits were recorded from the included experiments. Only 14 traits were measured on more than five occasions across studies. Traits within the biochemical, molecular and productive trait groups were reported most frequently in the published literature and were most affected by production diseases; among these were some cytokines (interleukin (IL) 1-ß, IL6, IL8 and tumour necrosis factor-α), acute phase proteins (haptoglobin) and daily weight gain. Quantification of the influence of factors relating to animal characteristics or husbandry practices was not possible, due to the low frequency of reporting throughout the literature. To conclude, this study has permitted a holistic assessment of traits measured in the published literature to study production diseases occurring in various stages of the production cycle of pigs. It shows the lack of consensus and common measurements of traits to characterise production diseases within the scientific literature. Specific traits, most of them relating to performance characteristics or immunological response of pigs, are proposed for further study as potential tools for the prognosis and study of production diseases.

Ciliostasis of airway epithelial cells facilitates influenza A virus infection.

Porcine precision-cut lung slices (PCLS) were used to analyze the effect of the ciliary activity on infection of airway epithelial cells by influenza viruses. Treatment of slices with 2% NaCl for 30 min resulted in reversible ciliostasis. When PCLS were infected by a swine influenza virus of the H3N2 subtype under ciliostatic conditions, the viral yield was about twofold or threefold higher at 24 or 48 h post-infection, respectively, as compared to slices with ciliary activity. Therefore, the cilia beating not only transports the mucus out of the airways, it also impedes virus infection.

Effects of feeding diets containing essential oils and betaine to heat-stressed growing-finishing pigs.

This study was to evaluate the effects of dietary essential oils (EO) and betaine on growth performance, nutrient digestibility and serum hormones in growing-finishing pigs under heat stress conditions. A total of 96 crossed pigs [(Landrace × Yorkshire) × Duroc] with an initial body weight (BW) of 24.7 ± 0.27 kg were used in an 18-week trial. Pigs were randomly allocated to four treatments according to BW and gender. There were six replication pens in each treatment, with four pigs (two barrows and two gilts) per pen. Treatment groups were: (1) control group (CON), basal diet + 23°C for 24 h; (2) heat stress group (HC) with basal diet + 37°C for 9 h, 23°C for 15 h; (3) group HEO, HC with 0.01% EO; (4) group HBE, HC with 0.1% betaine. During the overall period, groups HEO and HBE had higher (p < 0.05) average daily gain than group HC. At week 6, group HC had a lower apparent total tract digestibility (ATTD) of dry matter (DM) (p < 0.05), but at week 12, this group had lower ATTD of DM, nitrogen and gross energy than group HEO (p < 0.05). At week 12 and 18, dietary EO decreased (p < 0.05) serum cortisol and norepinephrine concentration. At week 18, dietary EO and betaine decreased (p < 0.05) epinephrine concentration. Conclusively, dietary EO may be a potential nutritional strategy to alleviate heat stress in growing-finishing pigs.

Porcine epidemic diarrhea virus through p53-dependent pathway causes cell cycle arrest in the G0/G1 phase.

Porcine epidemic diarrhea virus (PEDV), an enteropathogenic Alphacoronavirus, has caused enormous economic losses in the swine industry. p53 protein exists in a wide variety of animal cells, which is involved in cell cycle regulation, apoptosis, cell differentiation and other biological functions. In this study, we investigated the effects of PEDV infection on the cell cycle of Vero cells and p53 activation. The results demonstrated that PEDV infection induces cell cycle arrest at G0/G1 phase in Vero cells, while UV-inactivated PEDV does not cause cell cycle arrest. PEDV infection up-regulates the levels of p21, cdc2, cdk2, cdk4, Cyclin A protein and down-regulates Cyclin E protein. Further research results showed that inhibition of p53 signaling pathway can reverse the cell cycle arrest in G0/G1 phase induced by PEDV infection and cancel out the up-regulation of p21 and corresponding Cyclin/cdk mentioned above. In addition, PEDV infection of the cells synchronized in various stages of cell cycle showed that viral subgenomic RNA and virus titer were higher in the cells released from G0/G1 phase synchronized cells than that in the cells released from the G1/S phase and G2/M phase synchronized or asynchronous cells after 18 h p.i.. This is the first report to demonstrate that the p53-dependent pathway plays an important role in PEDV induced cell cycle arrest and beneficially contributes to viral infection.

Longitudinal Effects of Iron Deficiency Anemia and Subsequent Repletion on Blood Parameters and the Rate and Composition of Growth in Pigs.

Iron deficiency is reported as the most common nutrient deficiency worldwide. Due to rapid growth, infants are at particular risk for developing iron deficiency, which can easily progress to iron deficiency anemia (IDA), if not treated. The aim of this study was to determine the lasting effects of an early-life iron deficiency after a period of dietary iron repletion. Forty-two intact male pigs were fed, ad libitum, either control (CONT, 21.3 mg Fe/L) or iron-deficient (ID 2.72 mg Fe/L) milk replacer from postnatal day (PND) 2 to 32 (phase 1). From PND 33 to 61 (phase 2), all pigs were transitioned onto a series of industry-standard, iron-adequate diets. Blood was collected weekly from PND 7 to 28, and again on PND 35 and 56, and tissues were collected at either PND 32 or PND 61. At the end of phase 1, ID pigs exhibited reduced hematocrit (Hct; p < 0.0001) and hemoglobin (Hb; p < 0.0001) compared with CONT pigs, but neither Hct (p = 0.5968) nor Hb (p = 0.6291) differed between treatment groups after dietary iron repletion at the end of phase 2. Body weight gain was reduced (p < 0.0001) 58% at PND 32 in ID pigs compared with CONT pigs during phase 1, and this effect remained significant at the end of phase 2 (p = 0.0001), with ID pigs weighing 34% less than CONT pigs at PND 61. Analysis of peripheral protein and messenger RNA (mRNA) gene expression biomarkers yielded inconclusive results, as would be expected based on previous biomarker analyses across multiple species. These findings suggest that early-life iron status negatively influences blood parameters and growth performance, with dietary iron repletion allowing for full recovery of hematological outcomes, but not growth performance.

Maternal obesity aggravates the abnormality of porcine placenta by increasing N6-methyladenosine.

BACKGROUND: The growing prevalence of overweight or obese pregnancies shows an increasing risk for aberrant fetal growth and postnatal complications. Maternal obesity is associated with low birth weight (LBW) of piglets. However, the development of LBW from maternal obesity is not well understood. OBJECTIVE: This study attempts to investigate the novel RNA modification N6-methyladenosine (m6A) in the placenta tissues by using sows with high backfat thickness as a model for obese pregnancy. SUBJECTS/METHODS: Forty four placentas from eight sows (backfat thickness ≥21 mm) were divided into four groups by piglet weight, with group1 being LBW group (<1.0 kg), group2 (1.0-1.4 kg), group3 (1.4-1.6 kg), and group4 (>1.6 kg) as the comparative groups of normal birth weight. QPCR was used to measure the mRNA levels of the genes and western blot was used to test the content of proteins. At the same time, LC-MS/MS method was built to test the content of m6A modification in the placental RNA, and finally MeRIP-QPCR technology was employed to check the specific m6A modification in the key genes. RESULTS: Compared with the comparative groups, the expression levels of PPARγ, VEGFA, ABHD5, and GPR120 in both mRNA and protein decreased noticeably in the LBW group. It was also observed that the density of the H&E stained vessels became attenuated in LBW group. Importantly, for the first time, the increased m6A levels were found in LBW placentas. Lower protein level of FTO (the key demethylase of m6A) was observed in LBW placentas, whereas no difference was found among the four groups in the expression levels of METTL3, the main methyltransferase of m6A. By using MeRIP-QPCR technology, the m6A modification in PPARγ, VEGFA, ABHD5, and GPR120, as well as FTO, was considerably enhanced in the placentas from LBW group. CONCLUSION: We infer that in maternity obesity, the higher m6A modification displayed in the genes related to placental development, lipid metabolism and angiogenesis may result in the down regulation of these genes, which could be associated with m6A demethylase FTO.

A live gI/gE-deleted pseudorabies virus (PRV) protects weaned piglets against lethal variant PRV challenge.

Emerging pseudorabies virus (PRV) variant has led to frequent outbreaks of PRV infection among Bartha-K61-vaccinated swine population in Chinese swine farms and caused high mortality in pigs of all age since late 2011. Here, we generated a gE/gI-deleted PRV (rPRVXJ-delgI/gE-EGFP) based on PRV variant strain (PRV-XJ) through homologous DNA recombination. Compared to parental strain, rPRVXJ-delgI/gE-EGFP showed similar growth kinetics in vitro. Its safety and immunogenicity were evaluated in weaned piglets. Our results showed that piglets immunized with rPRVXJ-delgI/gE-EGFP did not exhibit any clinical symptoms, and a high level of gB-specific antibody was detected. After lethal challenge with variant PRV (PRV-FJ strain), all vaccinated piglets survived without showing any clinical symptoms except slight fever within 7 days post-challenge. In unvaccinated piglets, typical clinical symptoms of pseudorabies were observed, and the piglets were all died at 5 days post-challenge. These results indicated that a live rPRVXJ-delgI/gE-EGFP vaccine could be a maker vaccine candidate to control the currently epidemic pseudorabies in China.

The effect of porcine epidemic diarrhea (PED) on ovarian function and reproductive performance after weaning in Berkshire sows.

The purpose of this study was to investigate the ovarian condition at weaning and subsequent reproductive performance of Berkshire sows following an outbreak of PED. This study was conducted on a farrow-to-finish farm that experienced a PED outbreak beginning on January 6, 2014. Blood samples were collected at weaning from 19 to 20 sows every month from July 2013 until July 2014 to investigate the ovarian condition. The mean progesterone concentration was numerically higher during January 2014 than the other months, but this difference was not significant. The mean estradiol-17ß concentration was higher during January 2014 than during July and October 2013 (P < 0.05). In addition, reproductive performance was compared during January, February, and March before (2013) and after (2014) the PED outbreak. Sows that farrowed in January had higher preweaning mortality in 2014 than in 2013 (P < 0.05), but sows that farrowed in February and March had similar preweaning mortality in 2013 and 2014 (P > 0.10). Sows that farrowed between January and March 2014 had 15% lower farrowing rate than those that farrowed during the same months in 2013 (P < 0.05). In conclusion, our results demonstrate poorer reproductive performance of Berkshire sows after a PED outbreak compared with before the outbreak.

Disease behaviours of sows naturally infected with Taenia solium in Tanzania.

Neurocysticercosis (NCC) is a disease caused by the zoonotic parasite Taenia solium lodging in the central nervous system. Both humans and pigs can get NCC. The impact of the disease in pigs has so far been little explored. The aim of this study was to describe the effect of NCC on social and feeding behaviours as well as the pattern of activity as indicators of reduced welfare in naturally infected sows. In total 13 T. solium naturally infected and 15 non-infected control sows were videotaped for 2 consecutive weeks using close circuit television cameras at research facilities at Sokoine University of Agriculture, Morogoro, Tanzania. Videos were analysed at the beginning, in the middle and at the end of the 2 week recording period. For each time point, videos were analysed during feeding, while the enrichment was provided, and by recording every half an hour the sows' behaviours performed over the course of a whole day. Sows with NCC spent significantly less time at the feeding trough, especially during the second half of the feeding period. Infected sows were also more passive e.g. lying and standing still significantly more during a whole day period and showed social isolation compared to non-infected control sows by performing behaviours more distant to their nearest neighbour. Results of this study indicated that NCC changed the behaviour of infected sows. The behavioural changes are indicative of decreased welfare. Efforts to reinforce the animal welfare aspect are needed as this has so far been neglected.