ABSTRACT
Stress is known to disrupt the intestinal barrier and induce intestinal dysfunction. A critical role for gonadotropin inhibitory hormone (GnIH) in stress has emerged. However, whether GnIH mediates stress-induced intestinal dysfunction remains unknown. The present study explored this question through in vivo and in vitro experiments in hens. Our in vivo experiments showed that continuous intraperitoneal injection of GnIH not only significantly increased the concentration of stress hormones in serum, but also significantly elevated the mRNA expression of glucocorticoid receptor (GR) in the duodenum and jejunum. Moreover, morphological and molecular analyses revealed that GnIH disrupted the physical and chemical barriers of the intestine and dramatically increased inflammatory factor levels in the intestine and serum of hens. Interestingly, the microbiomics results showed that GnIH altered the structure and composition of the gut flora in the cecum, revealing an increased abundance of harmful intestinal bacteria such as Desulfovibrionaceae. Similar results were found in in vitro studies in which the GnIH-induced intestinal mucosal barrier was disrupted, and inflammation increased in jejunal explants, although no significant difference was found in the expression of GR between the control and GnIH groups. Our results demonstrated that GnIH not only directly damaged intestinal barriers and elevated intestinal inflammation but also mediated stress and microflora imbalance-induced intestinal function disorder, suggesting that GnIH is a potential therapeutic target for gut dysfunction, stress-induced intestinal function disorder, and inflammatory bowel disease in animals and humans.
Subject(s)
Chickens , Gastrointestinal Microbiome , Stress, Physiological , Animals , Chickens/physiology , Female , Gastrointestinal Microbiome/physiology , Hypothalamic Hormones/metabolism , Hypothalamic Hormones/genetics , Poultry Diseases/microbiology , Poultry Diseases/physiopathology , Avian Proteins/metabolism , Avian Proteins/genetics , Intestinal Diseases/veterinary , Intestinal Diseases/microbiologyABSTRACT
We aimed to determine the onset time of hypophosphatemic rickets and investigate the mechanism of motility impairment through adenosine triphosphate (ATP) production in goslings. Two hundred and sixteen 1-day-old male Jiangnan white geese were randomly divided into 3 groups, with 6 replicates and 12 geese per replicate. Birds were fed on 3 diets: a control diet (nonphytic phosphorus, NPP, 0.38%), a P-deficient diet (PD; NPP, 0.08%), and a high P diet (HP; NPP, 0.80%) for 14 d. Subsequently, all birds were shifted to the control diet for an additional 14 d. The cumulative incidence of lameness increased significantly (P < 0.01) starting on d 4, reaching over 80% on d 7 and 100% on d 12 in the PD group. Drinking and eating frequency decreased from d 4 and d 5, respectively, in the PD group compared to the other groups (most P < 0.01). The PD group exhibited shorter and narrower beaks, higher (worse) curvature scores of the beak and costochondral junctions, swelling caput costae, and dirtier feathers since d 4, in contrast to the control and HP groups (most P < 0.01). The HP had bigger (P < 0.05) beak and sternum sizes than the control groups on d 4 to 11. Leg muscle ATP levels were lower (P < 0.01 or 0.05) on d 4 to 11; in contrast, adenosine diphosphate (d 7-11) was higher in PD compared to the control (P < 0.05). Leg muscle ATP level had positive linear (R2 > 0.40) correlations (r > 0.60) with eating and drinking frequencies on d 7 and 11 (P < 0.01). Bone stiffness, feather cleanliness, and ATP levels recovered (P > 0.05) to the control level, whereas bone size did not recover (P < 0.05) in PD and HP after eating the control diet for 2 wk. The onset time of hypophosphatemic rickets was around 4 d in goslings, and insufficient leg muscle ATP was related to the impaired motility observed in early P-deficient geese.
Subject(s)
Adenosine Triphosphate , Animal Feed , Diet , Geese , Poultry Diseases , Animals , Male , Adenosine Triphosphate/metabolism , Geese/physiology , Diet/veterinary , Poultry Diseases/physiopathology , Animal Feed/analysis , Random Allocation , Muscle, Skeletal/metabolism , Phosphorus, Dietary/metabolism , Rickets/veterinary , Phosphorus/deficiency , Phosphorus/metabolismABSTRACT
Introduction: Refractile bodies (RB) are large membrane-less organelles (MLO) of unknown function found as a prominent mismatched pair within the sporozoite stages of all species of Eimeria, parasitic coccidian protozoa. Methods: High resolution imaging methods including time-lapse live confocal microscopy and serial block face-scanning electron microscopy (SBF-SEM) were used to investigate the morphology of RB and other intracellular organelles before and after sporozoite invasion of host cells. Results: Live cell imaging of MDBK cells infected with E. tenella sporozoites confirmed previous reports that RB reduce from two to one post-infection and showed that reduction in RB number occurs via merger of the anterior RB with the posterior RB, a process that lasts 20-40 seconds and takes place between 2- and 5-hours post-infection. Ultrastructural studies using SBF-SEM on whole individual sporozoites, both pre- and post-host cell invasion, confirmed the live cell imaging observations and showed also that changes to the overall sporozoite cell shape accompanied RB merger. Furthermore, the single RB post-merger was found to be larger in volume than the two RB pre-merger. Actin inhibitors were used to investigate a potential role for actin in RB merger, Cytochalasin D significantly inhibited both RB merger and the accompanying changes in sporozoite cell shape. Discussion: MLOs in eukaryotic organisms are characterised by their lack of a membrane and ability to undergo liquid-liquid phase separation (LLPS) and fusion, usually in an actin-mediated fashion. Based on the changes in sporozoite cell shape observed at the time of RB merger together with a potential role for actin in this process, we propose that RB are classed as an MLO and recognised as one of the largest MLOs so far characterised.
Subject(s)
Chickens , Coccidiosis , Eimeria tenella , Organelles , Poultry Diseases , Sporozoites , Animals , Actins/metabolism , Chickens/metabolism , Chickens/parasitology , Eimeria tenella/metabolism , Eimeria tenella/physiology , Organelles/metabolism , Organelles/physiology , Sporozoites/metabolism , Sporozoites/physiology , Coccidiosis/metabolism , Coccidiosis/parasitology , Coccidiosis/physiopathology , Poultry Diseases/metabolism , Poultry Diseases/parasitology , Poultry Diseases/physiopathologyABSTRACT
White chick hatchery disease is an emerging disease of broiler chicks with which the virus, chicken astrovirus, has been associated. Adult birds typically show no obvious clinical signs of infection, although some broiler breeder flocks have experienced slight egg drops. Substantial decreases in hatching are experienced over a two-week period, with an increase in mid-to-late embryo deaths, chicks too weak to hatch and pale, runted chicks with high mortality. Chicken astrovirus is an enteric virus, and strains are typically transmitted horizontally within flocks via the faecal-oral route; however, dead-in-shell embryos and weak, pale hatchlings indicate vertical transmission of the strains associated with white chick hatchery disease. Hatch levels are typically restored after two weeks when seroconversion of the hens to chicken astrovirus has occurred. Currently, there are no commercial vaccines available for the virus; therefore, the only means of protection is by good levels of biosecurity. This review aims to outline the current understanding regarding white chick hatchery disease in broiler chick flocks suffering from severe early mortality and increased embryo death in countries worldwide.
Subject(s)
Astroviridae Infections/veterinary , Avastrovirus , Chickens , Communicable Diseases, Emerging/veterinary , Poultry Diseases , Animal Husbandry , Animals , Astroviridae Infections/physiopathology , Astroviridae Infections/prevention & control , Astroviridae Infections/virology , Avastrovirus/isolation & purification , Communicable Diseases, Emerging/physiopathology , Communicable Diseases, Emerging/prevention & control , Communicable Diseases, Emerging/virology , Disease Progression , Poultry Diseases/physiopathology , Poultry Diseases/prevention & control , Poultry Diseases/virologyABSTRACT
Infectious bronchitis virus (IBV) infection causes significant economic losses to various sectors of the poultry industry worldwide. Over the past few years, the incidence of false layer syndrome in Eastern Canadian layer flocks has been associated with the increased prevalence of the IBV Delmarva (DMV)/1639 strain. In this study, 1-day-old specific-pathogen-free (SPF) hens were infected with the Canadian DMV/1639 strain and observed until 16 weeks of age in order to determine if the IBV DMV/1639 strain is causing false layer syndrome. Early after infection, the virus showed a wide tissue distribution with characteristic gross and histopathological lesions in the respiratory tract and kidney. Around 60-70% of the infected hens demonstrated continuous cloacal viral shedding until the end of the experiment (at 16 weeks) which was associated with high IBV genome loads detected in the cecal tonsils. The experiment confirmed the field observations that the Canadian DMV/1639 strain is highly pathogenic to the female reproductive tract causing marked cystic lesions in the oviduct. Moreover, significant histopathological damage was observed in the ovary. Our study provides a detailed description of the pathological consequences of the IBV DMV/1639 strain circulating in an important poultry production sector.
Subject(s)
Coronavirus Infections/veterinary , Infectious bronchitis virus/physiology , Infectious bronchitis virus/pathogenicity , Oviducts/virology , Poultry Diseases/virology , Animals , Chickens , Coronavirus Infections/pathology , Coronavirus Infections/physiopathology , Coronavirus Infections/virology , Female , Infectious bronchitis virus/genetics , Infectious bronchitis virus/isolation & purification , Oviducts/pathology , Poultry Diseases/pathology , Poultry Diseases/physiopathology , Reproduction , Specific Pathogen-Free Organisms , VirulenceABSTRACT
Salmonella enterica ssp. enterica serovars Enteritidis (SE) and Gallinarum (SG) cause different diseases in chickens. However, both are able to reach the blood stream where heterophils and monocytes are potentially able to phagocytose and kill the pathogens. Using an ex vivo chicken whole blood infection model, we compared the complex interactions of the differentially host-adapted SE and SG with immune cells in blood samples of two White Leghorn chicken lines showing different laying performance (WLA: high producer; R11: low producer). In order to examine the dynamic interaction between peripheral blood leucocytes and the Salmonella serovars, we performed flow cytometric analyses and survival assays measuring (i) leucocyte numbers, (ii) pathogen association with immune cells, (iii) Salmonella viability and (iv) immune gene transcription in infected whole blood over a four-hour co-culture period. Inoculation of blood from the two chicken lines with Salmonella led primarily to an interaction of the bacteria with monocytes, followed by heterophils and thrombocytes. We found higher proportions of monocytes associated with SE than with SG. In blood samples of high producing chickens, a decrease in the numbers of both heterophils and Salmonella was observed. The Salmonella challenge induced transcription of interleukin-8 (IL-8) which was more pronounced in SG- than SE-inoculated blood of R11. In conclusion, the stronger interaction of monocytes with SE than SG and the better survivability of Salmonella in blood of low-producer chickens shows that the host-pathogen interaction and the strength of the immune defence depend on both the Salmonella serovar and the chicken line.
Subject(s)
Chickens , Leukocytes/microbiology , Poultry Diseases/microbiology , Salmonella Infections, Animal/microbiology , Salmonella enteritidis/physiology , Salmonella/physiology , Animals , Female , Poultry Diseases/physiopathologyABSTRACT
In this study, changes in cloacal temperature and clinical manifestations due to very virulent infectious bursal disease virus (vvIBDV) infection in pigeons (Columba livia domestica) and transmission to chickens were demonstrated. Thirty pigeons (3-6 weeks old) and thirty chickens (3 weeks old) divided into 4 groups (I-IV) were used for this study. Group I comprised of 10 uninoculated pigeons only; II comprised of 10 inoculated pigeons and 10 sentinel chickens; III comprised of 10 sentinel pigeons and 10 inoculated chickens, while IV comprised of 10 uninoculated chickens only. Pigeons in group II and chickens in group III were each inoculated with 0.20 mL (titre of 109.76CID50/mL) of vvIBDV (Nigerian strain). Cloacal temperature was monitored and clinical manifestations scored post-inoculation (pi). Results indicated significant (P < 0.05) pyrexia at 2 days pi (dpi), mild clinical signs and no mortality in inoculated pigeons. Significant (P < 0.05) pyrexia at 2-4 dpi, severe clinical signs and mortality (50%; 60%) were observed in inoculated and sentinel chickens. IBDV antigen and antibody were detected in pigeons and chickens. Pigeons showed response to vvIBDV infection thus suggesting susceptibility of pigeons to IBD. Sentinel chickens presented clinical manifestations of IBD and this suggests transmission from pigeons to chickens. This study therefore documents pyrexia and clinical manifestations due to vvIBDV infection in pigeons and successful transmission of the virus between pigeons and chickens.
Subject(s)
Bird Diseases/virology , Birnaviridae Infections/veterinary , Chickens , Cloaca/physiology , Columbidae , Infectious bursal disease virus/pathogenicity , Animals , Bird Diseases/physiopathology , Bird Diseases/transmission , Birnaviridae Infections/physiopathology , Birnaviridae Infections/transmission , Birnaviridae Infections/virology , Infectious bursal disease virus/physiology , Poultry Diseases/physiopathology , Poultry Diseases/transmission , Poultry Diseases/virology , TemperatureABSTRACT
The study investigated the mitigating effects of two probiotics on blood parameters of ISA Brown chicks inoculated with a very virulent infectious bursal disease virus (vvIBDV). Two hundred chicks were assigned into four groups of 50 birds each. Groups A and B were administered Antox® in water and Bactofort® in feed daily from 1 to 42 days of age and inoculated with a vvIBDV at 28 days and C and D served as positive and negative controls, respectively. Blood samples were examined for changes in packed cell volume (PCV), haemoglobin concentration (Hb), red blood cell (RBC), total white blood cell (TWBC), heterophil and lymphocyte counts seven days post inoculation. The PCV between groups A and C differed (P < 0.05) and in group B it was higher (P < 0.05) than that of group C. The Hb concentration between groups A, B and C differed (P < 0.05). There was a difference (P < 0.05) in RBC counts between groups A, B, C. Differences in TWBC between group A and C were significant (P < 0.05) and TWBC in group B was higher (P < 0.05) than that of group C. There was a significant difference in heterophil (P < 0.05) and lymphocyte (P < 0.05) count between group A and C, and B and C. Heterophil/lymphocyte ratio was significantly higher in positive control compared to groups A, B, C. Antox® and Bactofort® mitigated the deleterious effects of vvIBDV on blood parameters and can assist in cases of IBD outbreak.
Subject(s)
Birnaviridae Infections/veterinary , Chickens , Infectious bursal disease virus/physiology , Poultry Diseases/blood , Probiotics/administration & dosage , Animals , Birnaviridae Infections/blood , Birnaviridae Infections/physiopathology , Birnaviridae Infections/virology , Poultry Diseases/physiopathology , Poultry Diseases/virologyABSTRACT
Physiological determinants of different body weight (BW) broiler chickens under heat stressed conditions were investigated to compare the performance at market age considering medium body weight group as standard. At 5 weeks, broilers were categorized randomly into 3 treatments (N = 24 per group) as high (HBW) (>1050 g), medium (MBW) (900-1050 g) and low (LBW) (<900 g) followed by simultaneous exposure to normal and heat stress (HS) conditions at 40 ± 1 °C and 45 ± 5% RH for 4 h/day for a period of 7 days (D) and sample collection was employed at D0, D3 and D7. Physiological and stress responses, haematological and biochemical profile, intestinal gross and histological aspects were estimated using standard protocols. Heart rate and mean arterial blood pressure were significantly (P = 0.000) higher in HBW broilers followed by low and medium ones. Heat stress exposure indicated significant (P = 0.000) increase in heart rate, arterial blood pressure, respiration rate and comb temperature while cloacal temperature remained unaffected. Lymphocytes, eosinophils, total red blood cell count, haemoglobin, and haematocrit were reduced (P = 0.000) whereas mean corpuscular volume and mean corpuscular hemoglobin, heterophil count and heterophil to lymphocyte ratio were increased (P = 0.000) in response to HS. Circulating corticosterone and tri-iodothyronine concentrations showed inverse relationship with respect to BW variation and HS duration respectively with significant interaction (P = 0.000). Higher protein in LBW was observed on D3. Serum triglycerides remained unaffected till D3 exposure but significantly (P = 0.017) reduced on D7 with lowest content in HBW group. Serum alkaline phosphatase increased in LBW group with significant heat stress interaction (P = 0.000) on D3. HS reduced villi length and crypt depth; but their corresponding ratio increased. In conclusion, HBW broilers are more affected than MBW or LBW groups. This study established interactive roles of BW and HS on physiological responses in broilers.
Subject(s)
Body Weight , Chickens/physiology , Heat Stress Disorders/physiopathology , Heat-Shock Response , Poultry Diseases/physiopathology , Alkaline Phosphatase/blood , Animals , Arterial Pressure , Chickens/blood , Corticosterone/blood , Heart Rate , Heat Stress Disorders/veterinary , Hematologic Tests , Hepatocytes/pathology , Stress, Physiological/physiologyABSTRACT
In the medulla of bursal follicle, only the secretory dendritic cell (BSDC) is furnished with secretory machinery. The granular discharge of BSDC appears in membrane-bound and solubilized forms. Movat pentachrome staining proves that the solubilized form is a glycoprotein, which fills up the extracellular space of follicular medulla. The glycoprotein contributes to bursal microenvironment and may be attached to the surface of medullary lymphocytes. The secretory granules of BSDC may be fused, resulting in large, irregular dense bodies, which are the first sign of BSDC transformation to macrophage-like cells (Mal). To determine the effect of infectious bursal disease virus (IBDV) infection on the extracellular glycoprotein and BSDC, SPF chickens were experimentally infected with IBDV. On the surface of BSDC, the secretory substance is in high concentration, which may contribute to primary binding of IBDV to BSDC. The early distribution of IBDV infected cells is in consent with that BSDC. The IBDV infected BSDC rapidly transforms to Mal in which the glycoprotein staining appears. In the dense bodies, the packed virus particles inhibit the virus particles preventing the granular discharge, which may represent the first, early phase of virus replication cycle. The absence of extracellular glycoprotein results in alteration in the medullary microenvironment and subsequently B cell apoptosis. On the surface of medullary B cells, the solubilized secretory substance can be in much lower concentration, which results in secondary binding of IBDV to B cells. In secondary, late phase of virus replication cycle, the virus particles are not packed in electron dense substance which results in cytolytic lymphocytes and presence of virus in extracellular space. The Mal emigrates into the cortex, where induces inflammation, recruiting heterophil granulocyte and monocyte.
Subject(s)
Birnaviridae Infections , Glycoproteins , Infectious bursal disease virus , Poultry Diseases , Animals , Birnaviridae Infections/physiopathology , Birnaviridae Infections/veterinary , Chickens , Glycoproteins/metabolism , Infectious bursal disease virus/metabolism , Lymphocytes/pathology , Poultry Diseases/physiopathologyABSTRACT
Intestinal development is closely associated with inflammatory wooden breast (WB) myopathy. Vitamin E (VE) and alpha lipoic acid (ALA) with antioxidant and anti-inflammatory effects were used independently and in combination to evaluate their effects on intestinal developmental changes in ileal morphology and expression of genes related with gut nutrient transport, structure, and inflammation in broilers during the first 3 wk posthatch. A total of 160 newly hatched Ross 708 broiler chicks were randomly assigned into a control and 3 dietary treatments with 10 replicates of 4 birds each. Supplementation of VE (160 mg/kg) and ALA (500 mg/kg) independently and in combination were fed during the first 3 wk. At 1, 2, and 3 wk of age, one chick from each pen was harvested. Plasma VE concentration and ileal morphology were determined. Gene expression was measured by real-time quantitative PCR. Broilers in VE and combination of ALA and VE group had higher plasma VE concentration than the control and ALA group at 1, 2, and 3 wk of age (P < 0.01). All dietary treatments increased ileal villus height at 1 wk of age (P < 0.01) and decreased intraepithelial lymphocytes at 3 wk of age compared to the control (P ≤ 0.05). Combination of VE and ALA increased collagen type IV alpha 1 chain expression (P ≤ 0.05) and improved basement membrane structure indicating increased gut basement membrane integrity at 2 and 3 wk of age compared to the control. Expression of lipopolysaccharide-induced tumor necrosis factor-alpha factor associated with inflammation was decreased in all dietary treatments at 3 wk of age compared to the control (P < 0.01). Ileal morphology and gene expression were closely correlated with breast muscle morphology and gene expression. These results suggest that VE and ALA especially when they were combined in the diet had positive effects on mitigating intestinal inflammation and improving nutrient transport beginning at 1 wk of age, which is likely critical in reducing the severity of WB.
Subject(s)
Chickens , Dietary Supplements , Intestines , Muscular Diseases , Poultry Diseases , Thioctic Acid , Vitamin E , Animals , Diet/veterinary , Intestines/drug effects , Intestines/embryology , Muscular Diseases/diet therapy , Muscular Diseases/physiopathology , Muscular Diseases/veterinary , Poultry Diseases/diet therapy , Poultry Diseases/physiopathology , Random Allocation , Thioctic Acid/pharmacology , Vitamin E/pharmacologyABSTRACT
Polyphasic myodegeneration potentially causes severe physiological and metabolic disorders in the breast muscle of fast-growing broiler chickens. To date, the etiology of recent muscle myopathies, such as the white striping (WS) phenotype, is still unknown. White striping-affected breast meats compromise the water holding capacity and predispose muscle to poor vascular tone, leading to the deterioration of meat qualities. Herein, this review article provides insight on the complexities around chicken breast myopathies: (i) the etiologies of WS occurrence in chicken; (ii) the metabolic changes that occur in WS defect in pectoralis major; and (iii) the interactions between breast muscle physiology and vascular tone. It also addressed the effects of nutritional supplements on muscle myopathies on chicken breast meats. Moreover, the review explored breast muscle biology focusing on the early preparation of satellite and vascular cells in fast-growth chicken breeds. Transcriptomics and histological analyses revealed poor vascularity in breast muscle of fast growth chickens. Thus, we suggest in ovo feeding of nutrients promoting vascularization and satellite cells replenishment as a potential strategy to enhance endothelium-derived nitric oxide availability to promote vascularization in the pectoralis major muscle region.
Subject(s)
Muscular Diseases , Pectoralis Muscles , Poultry Diseases , Animals , Chickens , Meat/standards , Muscular Diseases/physiopathology , Muscular Diseases/veterinary , Pectoralis Muscles/metabolism , Pectoralis Muscles/physiopathology , Poultry Diseases/physiopathologyABSTRACT
Riemerella anatipestifer causes epizootic infectious disease in poultry resulting in serious economic losses especially to the duck industry. In our previous study, R. anatipestifer was found to lyse duck erythrocytes in vitro. In the present study, a random Tn4351 mutagenesis library of hemolytic R. anatipestifer strain SX containing 4000 mutants was constructed to investigate the genetic basis of hemolytic activity. Thirty mutants with reduced hemolytic activity and one with increased hemolytic activity were screened and insertions in 24 genes were identified. Of these genes, four were predicted to encode outer membrane proteins, one encoded a cytoplasmic membrane protein, 11 encoded cytoplasmic proteins, and eight encoded proteins with unknown locations. Based on current annotations of the R. anatipestifer genomes, of the 24 genes, 7 (29.17%) were involved in iron utilization. The hemolytic activities of the complemented strains M2 (pRES-Riean_0790) and M18 (pRES-Riean_0653) were restored, indicating that both Riean_0653 and Riean_0790 are involved in the hemolytic activity of strain SX. However, the recombinant proteins rRiean_0317, rRiean_0790, rRiean_0653, rRiean_1027, rRiean_1143, and rRiean_1561 had no hemolytic activity, suggesting that none were hemolysins.
Subject(s)
DNA Transposable Elements/genetics , Ducks , Flavobacteriaceae Infections/veterinary , Hemolysis/genetics , Mutagenesis, Insertional , Poultry Diseases/physiopathology , Riemerella/genetics , Animals , Flavobacteriaceae Infections/microbiology , Flavobacteriaceae Infections/physiopathology , Poultry Diseases/microbiologyABSTRACT
Broiler ascites syndrome (AS), also called pulmonary artery hypertension, is a metabolic disorder that has been observed worldwide in fast-growing broilers. Pulmonary arterial remodeling is a key step in the development of AS. The precise relationship between mRNA and SNP of the pulmonary artery in regulating AS progression remains unclear. In this study, we obtained pulmonary artery tissues from broilers with AS to perform pathologic section and pathologic anatomic observation. SNP, InDel, and mRNA data analysis were carried out using GATK and ANNOVAR software to study the SNP loci of 985 previously reported genes (437 upregulated and 458 downregulated). The pathology results showed that there was a lot of yellow fluid in the abdominal cavity and pericardium, that the ascites cardiac index and hematocrit changed significantly, and that the pulmonary artery had remodeled and become thicker in the disease group. Myocardial sections showed vacuolar degeneration of myocytes and rupture of muscle fibers. In addition, ALDH7A1, IRG1, GGT5, IGSF1, DHX58, USP36, TREML2, SPAG1, CD34, and PLEKHA7 were found to be closely associated with the pathogenesis of pulmonary artery remodeling in AS progression. Taken together, our present study further illuminates the molecular mechanism of pulmonary artery remodeling underlying AS progression.
Subject(s)
Ascites , Chickens , Polymorphism, Single Nucleotide , Poultry Diseases , RNA, Messenger , Vascular Remodeling , Animals , Ascites/genetics , Ascites/physiopathology , Ascites/veterinary , Chickens/genetics , Polymorphism, Single Nucleotide/genetics , Poultry Diseases/genetics , Poultry Diseases/physiopathology , Pulmonary Artery/physiopathology , RNA, Messenger/genetics , Vascular Remodeling/geneticsABSTRACT
The primary cause of necrotic enteritis (NE) disease in chickens is the NetB-positive Clostridium perfringens bacterium. Many factors are known to affect the severity of NE in the challenge models of broiler chickens, and one of these factors is the virulence of C. perfringens strain. This study was conducted to evaluate the effect of 2 pathogenic C. perfringens strains in a NE challenge model on gut health and mRNA expression of genes encoding apoptosis, tight junction, immunity, and nutrient transporters in broilers. Day-old Ross-308 male broilers (n = 468) were allocated in a 2 × 3 factorial arrangement of treatments with in-feed antibiotics (no or yes) and challenge (Non, C. perfringens strain NE18, and C. perfringens strain NE36) as the factors. The birds in the challenged groups were inoculated with Eimeria species on day 9 and with a fresh suspension of C. perfringens NE18 or NE36 on day 14 and 15. Sample collection was performed on 2 birds of each pen on day 16. Necrotic enteritis challenge, impaired feed conversion ratio during day 0 to 16 compared with the control group where the effect of the NE36 challenge was more severe than that with NE18 (P < 0.001). The mRNA expression of mucin-2, immunoglobulin-G, occludin (P < 0.001), and tight junction protein-1 (P < 0.05) genes were downregulated in both challenged groups compared with the nonchallenged counterparts. Antibiotic supplementation, on the other hand, increased weight gain, and feed intake in all challenged birds (P < 0.01), but upregulated mucin-5ac and alanine, serine, cysteine, and threonine transporter-1 (P < 0.05) only in the NE18 challenged birds. The challenge with NE36 significantly upregulated caspase-8 and claudin-1 (P < 0.001), but downregulated glucose transporter-2 (P < 0.001) compared with the NE18 challenge. These results suggest that NE challenge is detrimental to the performance of broilers through compromised intestinal health, and different C. perfringens strains can affect the severity of the disease through modulating the expression of intestinal genes encoding proteins responsible for apoptosis, gut integrity, immunity, mucus production, and nutrient transporters.
Subject(s)
Clostridium Infections , Enteritis , Gene Expression Regulation , Poultry Diseases , Animal Feed/analysis , Animals , Chickens/genetics , Clostridium Infections/microbiology , Clostridium Infections/physiopathology , Clostridium Infections/veterinary , Clostridium perfringens/classification , Clostridium perfringens/pathogenicity , Enteritis/microbiology , Enteritis/physiopathology , Enteritis/veterinary , Gene Expression Profiling , Intestines/microbiology , Intestines/physiology , Male , Poultry Diseases/microbiology , Poultry Diseases/physiopathologyABSTRACT
Fatty liver diseases, common metabolic diseases in chickens, can lead to a decrease in egg production and sudden death of chickens. To solve problems caused by the diseases, reliable chicken models of fatty liver disease are required. To generate chicken models of fatty liver, 7-week-old ISA female chickens were fed with a control diet (17% protein, 5.3% fat, and 1,300 mg/kg choline), a low protein and high fat diet (LPHF, 13% protein, 9.1% fat, and 1,300 mg/kg choline), a high cholesterol with low choline diet (CLC, 17% protein, 7.6% fat with additional 2% cholesterol, and 800 mg/kg choline), a low protein, high fat, high cholesterol, and low choline diet (LPHFCLC, 13% protein, 12.6% fat with additional 2% cholesterol, and 800 mg/kg choline) for 4 wk. Our data showed that the CLC and LPHFCLC diets induced hyperlipidemia. Histological examination and the content of hepatic lipids indicated that the CLC and LPHFCLC diets induced hepatic steatosis. Plasma dipeptidyl peptidase 4, a biomarker of fatty liver diseases in laying hens, increased in chickens fed with the CLC or LPHFCLC diets. Hepatic ballooning and immune infiltration were observed in these livers accompanied by elevated interleukin 1 beta and lipopolysaccharide induced tumor necrosis factor mRNAs suggesting that the CLC and LPHFCLC diets also caused steatohepatitis in these livers. These diets also induced hepatic steatosis in Plymouth Rock chickens. Thus, the CLC and LPHFCLC diets can be used to generate models for fatty liver diseases in different strains of chickens. In ISA chickens fed with the CLC diet, peroxisome proliferator-activated receptor γ, sterol regulatory element binding transcription factor 1, and fatty acid synthase mRNAs increased in the livers, suggesting that lipogenesis was enhanced by the CLC treatment. Our data show that treatment with CLC or LPHFCLC for 4 wk induces fatty liver disease in chickens. These diets can be utilized to rapidly generate chicken models for fatty liver research.
Subject(s)
Chickens , Cholesterol , Choline , Diet , Fatty Liver , Hyperlipidemias , Animals , Cholesterol/metabolism , Choline/metabolism , Diet/veterinary , Disease Models, Animal , Fatty Liver/physiopathology , Fatty Liver/veterinary , Female , Hyperlipidemias/veterinary , Liver/pathology , Poultry Diseases/physiopathologyABSTRACT
Salmonella Pullorum is a pathogen specific to birds that can cause Pullorum disease in young chickens and lead to considerable economic losses in the poultry industry. During transmission and infection, S. Pullorum will encounter various environmental stresses and host defenses. The stringent response is an important adaptation response induced by (p)ppGpp, and in Salmonella, (p)ppGpp is synthesized by two (p)ppGpp synthetases, RelA and SpoT. To investigate the role of (p)ppGpp synthetases in the adaptation and pathogenicity of S. Pullorum, a (p)ppGpp synthetases mutant (ΔrelAΔspoT) was constructed, and its physiological phenotypes and pathogenicity, as well as transcription profiling, were compared with the parent strain. The ΔrelAΔspoT mutant showed decreased ability to form biofilms, and reduced resistance to acidic, alkaline, high osmolarity and H2O2 conditions. The internalization of the ΔrelAΔspoT mutant into host cells in vitro and its lethality and colonization abilities within young chickens were also significantly reduced. RNA sequencing showed that the (p)ppGpp synthetases did not only affect the classic stringent response, such as inhibition of DNA replication and protein synthesis, but also controlled the expression of many virulence factors, in particular, the Salmonella pathogenicity island 1 (SPI-1) and SPI-2 type III secretion systems (T3SSs), and adhesion factors. These results suggest that the (p)ppGpp synthetases are required for the pathogenicity of S. Pullorum by affecting its stress response and the expression of the virulence factors.
Subject(s)
Guanosine Pentaphosphate/genetics , Guanosine Pentaphosphate/metabolism , Salmonella Infections, Animal/microbiology , Salmonella/genetics , Salmonella/pathogenicity , Animals , Bacterial Proteins/genetics , Biofilms , Chickens/microbiology , Gene Deletion , Mice , Poultry Diseases/microbiology , Poultry Diseases/physiopathology , RAW 264.7 Cells , Salmonella/enzymology , Salmonella/growth & development , Specific Pathogen-Free Organisms , Virulence , Virulence Factors/geneticsABSTRACT
This study presents a case of clubbed down syndrome in conventional broilers. During the first week of life, severe growth retardation was observed in approximately 25% of the flock. The growth-retarded chicks weighed only 45â g and showed a typical feather disorder which was most apparent on their abdomen and was defined in literature as typical for clubbed down syndrome. Necropsies, histology, biochemical analysis of blood and liver samples, serology and different PCR tests were performed in broilers to assess the aetiology of the clinical signs that were present in the affected broiler farm. Because of the suspicion of a possible link with the broiler-breeder farms, different investigations including serology, PCR and feed analysis were also performed on these farms. The results suggest that an accidentally excessive amount of calcium and iron in the feed of broiler-breeders, 3 weeks prior to first clinical signs in broilers, led to the development of clubbed down in the offspring, because of a relative Zn-deficiency in broiler-breeders and an absolute Zn-deficiency in the hatching eggs that were produced during this period. This appeared to be a reversible process as no clinical signs were observed in younger offspring of these broiler-breeders after they had consumed more of the new batch of feed. A potential involvement of Astrovirus could not be completely ruled out. This study demonstrates the importance of correct mineral concentrations in broiler-breeder feed and the impact it can have on the development of the offspring.
Subject(s)
Animal Feed/analysis , Calcium/adverse effects , Chickens/growth & development , Down Syndrome/veterinary , Iron/adverse effects , Poultry Diseases/physiopathology , Zinc/deficiency , Animals , Body Weight , Breeding , Calcium/analysis , Chickens/physiology , Down Syndrome/physiopathology , Eating , Feathers/pathology , Female , Iron/analysis , MaleABSTRACT
BACKGROUND: Mycoplasma gallisepticum (MG) is the primary etiologic agent of chronic respiratory disease in poultry. However, the mechanism underlying MG-induced immune dysregulation in chicken is still elusive. Baicalin shows excellent anti-bacterial, anti-inflammatory, anti-carcinogenic and anti-viral properties. In the present study, the preventive effects of baicalin against immune impairment in chicken bursa of fabricius (BF) were studied in an MG infection model. RESULTS: Histopathological examination showed increased inflammatory cell infiltrations and fragmented nuclei in the model group. Ultrastructural analysis revealed the phenomenon of apoptosis in bursal cells, along with the deformation of mitochondrial membrane and swollen mitochondria in the model group. However, these abnormal morphological changes were partially alleviated by baicalin. Meanwhile, baicalin treatment attenuated the level of proinflammatory cytokines, and suppressed nuclear factor-kappa B expression at both protein and mRNA level. Terminal deoxynucleotidyl transferase-mediated dUTP nick endlabeling assay showed extensive apoptosis in BF in the model group. The mRNA and protein expression levels of apoptosis-related genes were upregulated in BF, while baicalin treatment significantly alleviated apoptosis in BF. In addition, alterations in mRNA and protein expression levels of autophagy-related genes and mitochondrial dynamics proteins were significantly alleviated by baicalin. Moreover, baicalin treatment significantly attenuated MG-induced decrease in CD8+ cells and reduced bacterial load in chicken BF compared to the model group. CONCLUSIONS: These results suggested that baicalin could effectively inhibit MG-induced immune impairment and alleviate inflammatory responses and apoptosis in chicken BF. © 2020 Society of Chemical Industry.
Subject(s)
Apoptosis/drug effects , Autophagy/drug effects , Bursa of Fabricius/immunology , Flavonoids/administration & dosage , Mycoplasma Infections/veterinary , Mycoplasma gallisepticum/physiology , Poultry Diseases/drug therapy , Animals , Bursa of Fabricius/cytology , Bursa of Fabricius/drug effects , Bursa of Fabricius/microbiology , Chickens , Mitochondria/genetics , Mitochondria/immunology , Mycoplasma Infections/drug therapy , Mycoplasma Infections/immunology , Mycoplasma Infections/physiopathology , NF-kappa B/genetics , NF-kappa B/immunology , Oxidative Stress/drug effects , Poultry Diseases/immunology , Poultry Diseases/physiopathologyABSTRACT
BACKGROUND: Heat stress seriously affects animal health and induces enormous financial losses in poultry production. Exploring the appropriate means for ameliorating unfavorable effects caused by heat stress is essential. We investigated whether taurine supplementation could attenuate breast muscle loss in chronic heat-stressed broilers, as well as its mechanism. We designed three groups: a normal control group (22 °C), a heat stress group (32 °C) and a taurine treatment group (32 °C, basal diet + 5 g·kg-1 taurine). RESULTS: We found that taurine significantly moderated the decreases of breast muscle mass and yield, as well as the increases of serum aspartate aminotransferase activity and serum urine acid level in chronic heat-stressed broilers. Additionally, supplementary taurine significantly alleviated elevations of the cytoplasm Ca2+ concentration, protein expressions of GRP78 and p-PERK, mRNA expressions of Ca2+ channels (RyR1, IP3R3) and endoplasmic reticulum (ER) stress factors (GRP78, GRP94, PERK, EIF2α, ATF4, IRE1, XBP1, ATF6 and CHOP), apoptosis (Caspase-3 and TUNEL), protein catabolism, and the reduction of taurine transporter (TauT) mRNA expression in the breast muscle induced by chronic heat stress. CONCLUSION: Supplementary taurine could attenuate chronic heat stress-induced breast muscle loss via reversing ER stress-induced apoptosis and suppressing protein catabolism. © 2020 Society of Chemical Industry.