Piglet Lungs Research Articles

Expression profiles of miRNAs in the lung tissue of piglets infected with Glaesserella parasuis and the roles of ssc-miR-135 and ssc-miR-155–3p in the regulation of inflammation

MicroRNAs (miRNAs) have been shown to play an important regulatory role in the process of pathogenic infection. However, the miRNAs that regulate the pathogenic process of G. parasuis and their functions are still unknown. Here, high-throughput sequencing was used to quantify the expression of miRNA in piglet lung tissue after G. parasuis XX0306 strain infection. A total of 25 differentially expressed microRNAs (DEmiRNAs) were identified. GO and KEGG pathway enrichment analysis showed that many of the functions of genes that may be regulated by DEmiRNA are related to inflammatory response and immune regulation. Further studies found that ssc-miR-135 may promote the expression of inflammatory factors through NF-κB signaling pathway. Whereas, ssc-miR-155–3p inhibited the inflammatory response induced by G. parasuis, and its regulatory mechanism remains to be further investigated. This study provides a valuable reference for revealing the regulatory effects of miRNAs on the pathogenesis of G. parasuis. Data AvailabilityThe datasets generated during the current study are not publicly available due to this study is currently in the ongoing research stage, and some of the data cannot be made public sooner yet, but are available from the corresponding author on reasonable request.

Pathogenicity Studies of NADC34-like Porcine Reproductive and Respiratory Syndrome Virus LNSY-GY and NADC30-like Porcine Reproductive and Respiratory Syndrome Virus GXGG-8011 in Piglets.

The porcine reproductive and respiratory syndrome virus (PRRSV) has caused significant economic losses to the swine industry. The U.S., China, and Peru have reported NADC30-like or NADC34-like PRRSV-infected piglets, which have been identified as the cause of a significant number of abortions in clinics. Although the pathogenicity of NADC30-like PRRSV and NADC34-like PRRSV in piglets exhibits significant variability globally, studies on their pathogenicity in China are limited. In this study, the animal experiments showed that within 8-14 days post-infection, both piglets infected with NADC30-like PRRSV GXGG-8011 and those infected with NADC34-like PRRSV LNSY-GY exhibited significant weight loss compared to the control piglets. Additionally, the viremia of the LNSY-GY persisted for 28 days, while the viremia of piglets infected with the GXGG-8011 lasted for 17 days. Similarly, the duration of viral shedding through the fecal-oral route after the LNSY-GY infection was longer than that observed after the GXGG-8011 infection. Furthermore, post-infection, both the LNSY-GY and GXGG-8011 led to pronounced histopathological lesions in the lungs of piglets, including interstitial pneumonia and notable viral colonization. However, the antibody production in the LNSY-GY-infected group occurred earlier than that in the GXGG-8011-infected group. Our research findings indicate that LNSY-GY is a mildly pathogenic strain in piglets, whereas we speculate that the GXGG-8011 might be a highly pathogenic strain.

High-dimensional analysis reveals an immune atlas and novel neutrophil clusters in the lungs of model animals with Actinobacillus pleuropneumoniae-induced pneumonia

Due to the increase in bacterial resistance, improving the anti-infectious immunity of the host is rapidly becoming a new strategy for the prevention and treatment of bacterial pneumonia. However, the specific lung immune responses and key immune cell subsets involved in bacterial infection are obscure. Actinobacillus pleuropneumoniae (APP) can cause porcine pleuropneumonia, a highly contagious respiratory disease that has caused severe economic losses in the swine industry. Here, using high-dimensional mass cytometry, the major immune cell repertoire in the lungs of mice with APP infection was profiled. Various phenotypically distinct neutrophil subsets and Ly-6C+ inflammatory monocytes/macrophages accumulated post-infection. Moreover, a linear differentiation trajectory from inactivated to activated to apoptotic neutrophils corresponded with the stages of uninfected, onset, and recovery of APP infection. CD14+ neutrophils, which mainly increased in number during the recovery stage of infection, were revealed to have a stronger ability to produce cytokines, especially IL-10 and IL-21, than their CD14− counterparts. Importantly, MHC-II+ neutrophils with antigen-presenting cell features were identified, and their numbers increased in the lung after APP infection. Similar results were further confirmed in the lungs of piglets infected with APP and Klebsiella pneumoniae infection by using a single-cell RNA-seq technique. Additionally, a correlation analysis between cluster composition and the infection process yielded a dynamic and temporally associated immune landscape where key immune clusters, including previously unrecognized ones, marked various stages of infection. Thus, these results reveal the characteristics of key neutrophil clusters and provide a detailed understanding of the immune response to bacterial pneumonia.

Adh Promotes Actinobacillus pleuropneumoniae Survival in Porcine Alveolar Macrophages by Inhibiting CHAC2-Mediated Respiratory Burst and Inflammatory Cytokine Expression.

Actinobacillus pleuropneumoniae (A. pleuropneumoniae) causes porcine pleuropneumonia that seriously endangers pig's health. Adh, located in the head region of trimeric autotransporter adhesion of A. pleuropneumoniae, affects bacterial adhesion and pathogenicity. However, how Adh mediates A. pleuropneumoniae immune invasion is still unclear. Here, we established the A. pleuropneumoniae strain L20 or L20 ΔAdh-infected porcine alveolar macrophages (PAM) model, and applied protein overexpression, RNA interference, qRT-PCR, Western blot and immunoflourescence techniques to dissect the effects of Adh on PAM during A. pleuropneumoniae infection. We found that Adh could increase the A. pleuropneumoniae adhesion and intracellular survival in PAM. Gene chip analysis of piglet lungs further showed that Adh significantly induced cation transport regulatory-like protein 2 (CHAC2) expression, whose overexpression suppressed the phagocytic capacity of PAM. Furthermore, CHAC2 overexpression dramatically increased glutathione (GSH) expression, decreased reactive oxygen species (ROS), and promoted A. pleuropneumoniae survival in PAM, while the knockdown of CHAC2 reversed these phenomena. Meanwhile, CHAC2 silence activated the NOD1/NF-κB pathway, resulting in an increase in IL-1β, IL-6, and TNF-α expression, whereas this effect was weakened by CHAC2 overexpression and addition of NOD1/NF-κB inhibitor ML130. Moreover, Adh enhanced the secretion of LPS of A. pleuropneumoniae, which regulated the expression of CHAC2 via TLR4. In conclusion, through a LPS-TLR4-CHAC2 pathway, Adh inhibits respiratory burst and inflammatory cytokines expression to promote A. pleuropneumoniae survival in PAM. This finding may provide a novel target for the prevention and treatment of A. pleuropneumoniae.

N-Acetylcysteine Administration Improves the Redox and Functional Gene Expression Levels in Spleen, Mesenteric Lymph Node and Gastrocnemius Muscle in Piglets Infected with Porcine Epidemic Diarrhea Virus.

Our previous study reported that N-acetylcysteine (NAC) administration improved the function of intestinal absorption in piglets infected with porcine epidemic diarrhea virus (PEDV). However, the effects of NAC administration on the functions of other tissues and organs in PEDV-infected piglets have not been reported. In this study, the effects of NAC on the liver, spleen, lung, lymph node, and gastrocnemius muscle in PEDV-infected piglets were investigated. Thirty-two 7-day-old piglets with similar body weights were randomly divided into one of four groups: Control group, NAC group, PEDV group, and PEDV+NAC group (eight replicates per group and one pig per replicate). The trial had a 2 × 2 factorial design consisting of oral administration of 0 or 25 mg/kg body weight NAC and oral administration of 0 or 1.0 × 104.5 TCID50 PEDV. The trial lasted 12 days. All piglets were fed a milk replacer. On days 5-9 of the trial, piglets in the NAC and PEDV + NAC groups were orally administered NAC once a day; piglets in the control and PEDV groups were orally administered the same volume of saline. On day 9 of trial, piglets in the PEDV and PEDV+NAC groups were orally administrated 1.0 × 104.5 TCID50 PEDV, and the piglets in the control and NAC groups were orally administrated the same volume of saline. On day 12 of trial, samples, including of the liver, spleen, lung, lymph node, and gastrocnemius muscle, were collected. PEDV infection significantly increased catalase activity but significantly decreased the mRNA levels of Keap1, Nrf2, HMOX2, IFN-α, MX1, IL-10, TNF-α, S100A12, MMP3, MMP13, TGF-β, and GJA1 in the spleens of piglets. NAC administration ameliorated abnormal changes in measured variables in the spleens of PEDV-infected piglets. In addition, NAC administration also enhanced the antioxidant capacity of the mesenteric lymph nodes and gastrocnemius muscles in PEDV-infected piglets. Collectively, these novel results revealed that NAC administration improved the redox and functional gene expression levels in the spleen, mesenteric lymph nodes, and gastrocnemius muscle in PEDV-infected piglets.

Congenital heart disease-associated pulmonary dysplasia and its underlying mechanisms.

Clinical observation indicates that exercise capacity, an important determinant of survival in patients with congenital heart disease (CHD), is most decreased in children with reduced pulmonary blood flow (RPF). However, the underlying mechanism remains unclear. Here, we obtained human RPF lung samples from children with tetralogy of Fallot as well as piglet and rat RPF lung samples from animals with pulmonary artery banding surgery. We observed impaired alveolarization and vascularization, the main characteristics of pulmonary dysplasia, in the lungs of RPF infants, piglets, and rats. RPF caused smaller lungs, cyanosis, and body weight loss in neonatal rats and reduced the number of alveolar type 2 cells. RNA sequencing demonstrated that RPF induced the downregulation of metabolism and migration, a key biological process of late alveolar development, and the upregulation of immune response, which was confirmed by flow cytometry and cytokine detection. In addition, the immunosuppressant cyclosporine A rescued pulmonary dysplasia and increased the expression of the Wnt signaling pathway, which is the driver of postnatal lung development. We concluded that RPF results in pulmonary dysplasia, which may account for the reduced exercise capacity of patients with CHD with RPF. The underlying mechanism is associated with immune response activation, and immunosuppressants have a therapeutic effect in CHD-associated pulmonary dysplasia.

Positive end expiratory pressure and respiratory system resistance between self-inflating bag and T-piece resuscitator in a cadaveric piglet lung model.

In neonatal resuscitation, T-piece resuscitator (TPR) are used widely, but the evidence is limited for their use in infants born at term gestation. The aim of this study was to compare the delivered positive end expiratory pressure (PEEP) and respiratory system resistance (Rrs) using TPR and self-inflating bag (SIB) in a cadaveric piglet model. Cadaveric newborn piglets were tracheotomised, intubated (cuffed tube) and leak tested. Static lung compliance was measured. Positive pressure ventilation was applied by TPR and SIB in a randomized sequence with varying, inflations per minute (40, 60 and 80 min) and peak inspiratory pressures (18 and 30 cmH2O). PEEP was constant at 5 cmH2O. The lungs were washed with saline and static lung compliance was re-measured; ventilation sequences were repeated. Lung inflation data for the respiratory mechanics were measured using a respiratory function monitor and digitally recorded for both pre and post-lung wash inflation sequences. A paired sample t-test was used to compare the mean and standard deviation. The mean difference in PEEP (TPR vs. SIB) was statistically significant at higher inflation rates of 60 and 80 bpm. At normal lung compliance, mean difference was 1.231 (p = 0.000) and 2.099 (p = 0.000) with PIP of 18 and 30 cmH2O respectively. Significantly higher Rrs were observed when using a TPR with higher inflation rates of 60 and 80 bpm at varying lung compliance. TPR is associated with significantly higher PEEP in a compliant lung model, which is probably related to the resistance of the TPR circuit. The effect of inadvertent PEEP on lung mechanics and hemodynamics need to be examined in humans. Further studies are needed to assess devices used to provide PEEP (TPR, SIB with PEEP valve, Anaesthetic bag with flow valve) during resuscitation of the newborn.

Alterations in the expression level of visfatin in the lungs of piglets infected with PRRSV and its effect on PRRSV replication

Porcine reproductive and respiratory syndrome (PRRS) is a highly contagious disease caused by PRRS virus (PRRSV), characterized by sow reproductive failure and respiratory symptoms in pigs of all ages. PRRSV mainly causes severe lung damage by invading alveolar macrophages. Visfatin is closely related to acute lung injury, immune response and inflammation along with virus invasion to the host. Therefore, the current study was performed to clarify the relationship between visfatin and PRRSV infection. We used ternary piglets to construct a piglet model to explore the expression of visfatin and tight junction protein in lung injury induced by PRRSV infection, and then further studied the inhibition effect of visfatin on PRRSV replication by PRRSV infection of Marc-145 cells. Our results indicated that both PRRSV attenuated and virulent infections could damage the lung tissues, which could not only lead to severe inflammatory reaction (such as increased expression of TNF-α, TGF-β, IL-8 and IL-10) in lung tissues of piglets, but also brought about the sharp decrease of ZO-1 and Tricellulin expressions resulting in impaired alveolar epithelial barrier. Meanwhile, we found significantly up-regulated expression of visfatin in lungs and serum of pigs after PRRSV infection that were related to both the degree of lung injury and the virulence of PRRSV strain. Moreover, visfatin might inhibit the PRRSV infection to Marc-145 cells in time dependent fashion. Hence, the current investigation provides the novel information about the effect of visfatin and PRRSV co-culture on Marc-145 cells and the effect of visfatin on PRRSV proliferation at different time points.

Transcriptome profiling identifies immune response genes against porcine reproductive and respiratory syndrome virus and Haemophilus parasuis co-infection in the lungs of piglets

Transcriptome profiling identifies immune response genes against porcine reproductive and respiratory syndrome virus and <i>Haemophilus parasuis</i> co-infection in the lungs of piglets

Transcriptome profiling identifies immune response genes against porcine reproductive and respiratory syndrome virus and Haemophilus parasuis co-infection in the lungs of piglets.

BackgroundCo-infections of the porcine reproductive and respiratory syndrome virus (PRRSV) and the Haemophilus parasuis (HPS) are severe in Chinese pigs, but the immune response genes against co-infected with 2 pathogens in the lungs have not been reported.ObjectivesTo understand the effect of PRRSV and/or HPS infection on the genes expression associated with lung immune function.MethodsThe expression of the immune-related genes was analyzed using RNA-sequencing and bioinformatics. Differentially expressed genes (DEGs) were detected and identified by quantitative real-time polymerase chain reaction (qRT-PCR), immunohistochemistry (IHC) and western blotting assays.ResultsAll experimental pigs showed clinical symptoms and lung lesions. RNA-seq analysis showed that 922 DEGs in co-challenged pigs were more than in the HPS group (709 DEGs) and the PRRSV group (676 DEGs). Eleven DEGs validated by qRT-PCR were consistent with the RNA sequencing results. Eleven common Kyoto Encyclopedia of Genes and Genomes pathways related to infection and immune were found in single-infected and co-challenged pigs, including autophagy, cytokine-cytokine receptor interaction, and antigen processing and presentation, involving different DEGs. A model of immune response to infection with PRRSV and HPS was predicted among the DEGs in the co-challenged pigs. Dual oxidase 1 (DUOX1) and interleukin-21 (IL21) were detected by IHC and western blot and showed significant differences between the co-challenged pigs and the controls.ConclusionsThese findings elucidated the transcriptome changes in the lungs after PRRSV and/or HPS infections, providing ideas for further study to inhibit ROS production and promote pulmonary fibrosis caused by co-challenging with PRRSV and HPS.

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.

Preliminary Experimental Study of Establishing a Lung Development Model with Specific Pathogen Free Preterm Pigs

To determine the best time for conducting cesarean section for the establishment of an animal model of lung development with specific pathogen free (SPF) preterm Bama minipigs under the condition of not making medical interventions such as hyperoxia, mechanical ventilation, or medication. SPF Bama sows at gestational day (GD) 113, GD107, GD104, GD101, and GD98 were selected and cesarean sections were performed. Then, the viability of the preterm piglets were observed. Based on their general data, viability, and paraffin sections stained with hematoxylin and eosin, the best time for performing cesarean section in order to build a SPF preterm pig model of lung development was determined. Cesarean sections were performed on a total of 7 sows and 55 piglets were delivered, among which 25 were still alive 3 hours after delivery. Seven piglets of GD104 and all piglets of GD107 and GD113 survived, while piglets of GD98 and GD101 all died. The survival rate of piglets of GD104 was 33.33% (7/21). Piglets of GD98 already possessed fully developed physical appearance and lung shape. Piglets from GD104 had better lung expansion and higher density of thin-walled alveoli. The lungs of GD107 piglets were basically fully expanded, and the density of thin-walled alveoli was almost the same as that of normal full-term piglets. Findings of this study suggest that SPF preterm piglets of GD104 with no specific pathogen exposure and no medical intervention can be used to establish a SPF preterm pig model of lung development.

Pathophysiological effects of intravenous phosphodiesterase type 4 inhibitor in addition to surfactant lavage in meconium-injured newborn piglet lungs.

Nonsteroidal anti-inflammatory drugs, such as selective phosphodiesterase type 4 (PDE4) inhibitors have potential anti-inflammatory and respiratory smooth muscle relaxation effects. This study aimed to investigate the pathophysiological effects of an intravenous PDE4 inhibitor (rolipram) and surfactant lavage (SL) in a newborn piglet model of meconium aspiration syndrome (MAS). MAS was induced in 25 newborn piglets, which were randomly divided into control and four SL treatment groups administered with different doses of intravenous rolipram (0, 0.1, 0.5, and 1 mg/kg). Cardiopulmonary variables were monitored and recorded. The experimental time was 4 hours. Serial blood was drawn for blood gas and biomarker analyses. Lung tissue was examined for histological analysis. All SL-treated groups revealed improved oxygenation during the 4-hour experiments and had significantly lower peak inspiratory pressure levels than the control group at the end of experiments. All SL plus rolipram-treated groups exhibited significantly higher lung compliance than the control group. However, the animals receiving high-dose (0.5 and 1.0 mg/kg) rolipram demonstrated significantly elevated heart rates. Lung histology of the nondependent sites revealed significantly lower lung injury scores in all SL-treated groups compared with that in the control group, but there were no differences among the rolipram-treated groups. In addition to SL, intravenous PDE4 inhibitors may further improve lung compliance in treating MAS; however, it is necessary to consider cardiovascular adverse effects, primarily tachycardia. Further investigations are required before the clinical application of intravenous PDE4 inhibitor as an anti-inflammatory agent to treat severe MAS.

Pathomorphological changes in the organs of neonatal piglets during feed contamination with mycotoxins for sows

Pathomorphological study of the neonatal period piglets of ontogenesis from the pig breeding complex obtained from sows that were given feed contaminated with mycotoxins during pregnancy and after parturition was carried out. Pathological changes in the internal organs of piglets, characterized by various dystrophic and inflammatory processes resulting from the influence of mycotoxins, were established. Edema and congestion in the lungs of piglets is noted as a sign of circulation failure in the body. Signs of interstitial pneumonia are detected with areas of chronic alveolar emphysema and atelectasis. Signs of granular dystrophy were noted in the heart in cardiomyocytes. Interstitial connective tissue has signs of edema; the swelling of blood vessel walls is noted. The morphofunctional state of the thyroid gland in piglets, taking into account changes in the organ structure, is characterized as a macro-microfollicular proliferating colloid goiter. The border smoothness between white and red pulp, hyperemia of blood vessels and the small number of lymphatic nodules with a size decrease are noted in the spleen. The demarcation clarity of white pulp into separate structural zones is not diagnosed in lymphatic nodules. Signs of catarrhal enteritis and chronic catarrhal colitis with a tendency to its transition to atrophic catarrh are detected in the small and large intestines of the gastrointestinal tract. Hepatocytes have mild signs of granular dystrophy in the lobules of the piglets’ liver. Protein hepatosis signs interspersed with areas of necrobiosis are identified in separate lobules of the organ against the background of general atrophy of hepatocytes. Granular dystrophy signs with the phenomena of its desquamation in certain areas are revealed in the convoluted tubules of kidney nephrons in epithelial cells. Part of epithelial cells of the nephron tubule is subject to necrobiotic processes. Thickening of the basic capillary membrane with glomerulitis is noted in the glomerulus of the renal corpuscle. Edema and mild lymphocyte-macrophage infiltration with the phenomena of the mucoid swelling of blood vessel walls is observed in the interstitial organ tissue.

Susceptibility of porcine pulmonary microvascular endothelial cells to porcine reproductive and respiratory syndrome virus.

Microvascular endothelial cells possess versatile functions and their roles in a variety of viral infections have been documented. Porcine reproductive and respiratory syndrome virus (PRRSV) infection induces severe lung inflammatory lesions in piglets, which is manifested as pulmonary endothelial dysfunction. However, the underlying mechanism of PRRSV affecting porcine pulmonary microvascular endothelial cells (PMECs) remains unknown. This study aimed to evaluate the susceptibility of PMECs to PRRSV. Primary PMECs were isolated and purified from piglet lungs, and the expression of three PRRSV receptors was characterized using immunofluorescence. Overt cytopathic effects of the PRRSV strain HN in PMECs were observed at day five post-infection, and PRRSV antigens in PMECs were determined at both RNA and protein levels using immunofluorescence and quantitative RT-PCR assays. The viral antigen significantly increased at 96 hr post-infection, and infectious virus was recovered from the supernatant of the infected PMECs. The results show that PMECs can be infected with the PRRSV strain HN, and that their receptor expression pattern is different from that of alveolar macrophages. The results of this study shed light on the potential roles of PMECs in PRRSV infection and provide a comprehensive understanding of the pathogenesis underlying its severe manifestation.

ITRAQ-based quantitative proteomics reveals the first proteome profiles of piglets infected with porcine circovirus type 3

Porcine circovirus type 3 (PCV3) infection induces porcine dermatitis and nephropathy syndrome, reproductive failure, and multisystemic inflammatory lesions in piglets and sows. To better understand the host responses to PCV3 infection, isobaric tags for relative and absolute quantification (iTRAQ) labeling combined with LC-MS/MS analysis was used for quantitative determination of differentially regulated cellular proteins in the lungs of specific-pathogen-free piglets after 4 weeks of PCV3 infection. Totally, 3429 proteins were detected in three independent mass spectrometry analyses, of which 242 differential cellular proteins were significantly regulated, consisting of 100 upregulated proteins and 142 downregulated proteins in PCV3-infected group relative to control group. Bioinformatics analysis revealed that these higher or lower abundant proteins involved primarily metabolic processes, innate immune response, MHC-I and MHC-II components, and phagosome pathways. Ten genes encoding differentially regulated proteins were selected for investigation via real-time RT-PCR. The expression levels of six representative proteins, OAS1, Mx1, ISG15, IFIT3, SOD2, and HSP60, were further confirmed by Western blotting and immunohistochemistry. This study attempted for the first time to investigate the protein profile of PCV3-infected piglets using iTRAQ technology; our findings provide valuable information to better understand the mechanisms underlying the host responses to PCV3 infection in piglets. SignificanceOur study identified differentially abundant proteins related to a variety of potential signaling pathways in the lungs of PCV3-infected piglets. These findings provide valuable information to better understand the mechanisms of host responses to PCV3 infection.

Influence of pig gut microbiota on Mycoplasma hyopneumoniae susceptibility

This study investigated the influence of gut microbiome composition in modulating susceptibility to Mycoplasma hyopneumoniae in pigs. Thirty-two conventional M. hyopneumoniae free piglets were randomly selected from six different litters at 3 weeks of age and were experimentally inoculated with M. hyopneumoniae at 8 weeks of age. Lung lesion scores (LS) were recorded 4 weeks post-inoculation (12 weeks of age) from piglet lungs at necropsy. Fecal bacterial community composition of piglets at 3, 8 and 12 weeks of age were targeted by amplifying the V3–V4 region of the 16S rRNA gene. The LS ranged from 0.3 to 43% with an evident clustering of the scores observed in piglets within litters. There were significant differences in species richness and alpha diversity in fecal microbiomes among piglets within litters at different time points (p < 0.05). The dissimilarity matrices indicated that at 3 weeks of age, the fecal microbiota of piglets was more dissimilar compared to those from 8 to 12 weeks of age. Specific groups of bacteria in the gut that might predict the decreased severity of M. hyopneumoniae associated lesions were identified. The microbial shift at 3 weeks of age was observed to be driven by the increase in abundance of the indicator family, Ruminococcaceae in piglets with low LS (p < 0.05). The taxa, Ruminococcus_2 having the highest richness scores, correlated significantly between litters showing stronger associations with the lowest LS (r = −0.49, p = 0.005). These findings suggest that early life gut microbiota can be a potential determinant for M. hyopneumoniae susceptibility in pigs.

Effect of porcine circovirus type 2 on the severity of lung and brain damage in piglets infected with porcine pseudorabies virus

Porcine circovirus type 2 (PCV2) is widespread throughout Chinese farms, and the infection rate of porcine pseudorabies virus (PRV) is very high. The emergence of mixed infection involving PCV2 and PRV has been difficult to prevent and control and has caused considerable economic loss. The present study investigated lung and brain damage caused by PRV in piglets with PCV2 infection. Twenty piglets were divided randomly into two experiment groups (PRV group and PRV + PCV2 group; n = 10 per group). The pigs were observed for clinical signs at specified times. At necropsy, lung and brain tissue samples were collected for histopathological examination, and tissue virus load was determined using quantitative polymerase chain reaction. Severe pathogenicity due to PRV was evident in two-month-old piglets. PCV2 and PRV co-infection led to more severe neurological and respiratory symptoms and a higher mortality rate in the piglets. In addition, the pathological damage to the lung and brain was also aggravated. The co-infection was associated with a significant increase in the content of PRV in the brain and lung tissue. In conclusion, PCV2 and PRV co-infection could cause severe and irreversible damage to piglets.

Effects of intratracheal captopril on severely meconium-injured piglet lungs.

Severe meconium aspiration syndrome (MAS) may cause intractable respiratory failure in neonates. Targeting the renin-angiotensin system may be an effective way to treat such pulmonary dysfunction. Captopril has the potential to mitigate the severity of lung injury by inhibiting angiotensin-converting enzyme. Twelve newborn piglets were intratracheally instilled with human meconium to induce severe MAS and were randomly treated with IT administration of captopril (0.5 mg/kg) (IT-Cap group, n = 6), or sham air instillation (Control group, n = 6). Cardiopulmonary profiles were monitored for a total of 5 hours. Pulmonary history was examined to compare lung injury severity between groups. There were no significant differences between the two study groups in gas exchange and lung compliance, peak inspiratory pressure, heart rate, and mean arterial blood pressure over the 5-h experimental period, but there were trends toward lower blood pressure and pH in the IT-Cap group. Histopathological examinations revealed significantly higher lung injury scores in the dependent site of the control group than in the nondependent site of the control group and both sites of the IT-Cap group. Intratracheal captopril did not present significant beneficial effects on severe meconium-injured lungs within 5 hours after injury. Further studies with different disease severities and dosing strategies are required.

What is happening in the ARDS piglet lungs: - the origin of B-lines on ultrasonography -

What is happening in the ARDS piglet lungs: - the origin of B-lines on ultrasonography -