Marek’s disease (MD) is a highly contagious pathogenic and oncogenic disease primarily affecting chickens. However, the mechanisms of genetic resistance for MD are complex and not fully understood. MD-resistant line 6₃ and MD-susceptible line 7₂ are two highly inbred progenitor lines of White Leghorn. Recombinant Congenic Strains (RCS) were developed from these two lines, which show varied susceptibility to MD. We investigated genetic structure and genomic signatures across the genome, including the line 6₃ and line 7₂, six RCSs, and two reciprocally crossed flocks between the lines 6₃ and 7₂ (F1 6₃ × 7₂ and F1 7₂ × 6₃) using Affymetrix® Axiom® HD 600 K genotyping array. We observed 18 chickens from RCS lines were specifically clustered into resistance sub-groups distributed around line 6₃. Additionally, homozygosity analysis was employed to explore potential genetic components related to MD resistance, while runs of homozygosity (ROH) are regions of the genome where the identical haplotypes are inherited from each parent. We found several genes including SIK, SOX1, LIG4, SIK1 and TNFSF13B were contained in ROH region identified in resistant group (line 6₃ and RCS), and these genes have been reported that are contribute to immunology and survival. Based on F_ST based population differential analysis, we also identified important genes related to cell death and anti-apoptosis, including AKT1, API5, CDH13, CFDP and USP15, which could be involved in divergent selection during inbreeding process. Our findings offer valuable insights for understanding the genetic mechanism of resistance to MD and the identified genes could be considered as candidate biomarkers in further evaluation.

Alloantigen systems are a broad group of molecules found on various cell types, including erythrocytes and lymphocytes. These alloantigens, identifie

This study compares kinetic parameters of Salmonella and surrogate Enterococcus faecium in mash broiler feed during thermal inactivation. Two-gram samples of mash broiler feed were added into a filtered sample bag and inoculated with nalidixic acid (NaL, 200 ppm) resistant S. Typhimurium or Enterococcus faecium, followed by vacuum-packaging and heating in a circulated thermal water bath at 75°, 85°, and 95°C for 0 to 180 s. Counts of bacterial survival were analyzed on tryptic soy agar and bile esculin agar plus 200 ppm of NaL. Microbial data and thermal kinetic parameters (n = 8, Global-Fit and United States Department of Agriculture [USDA]-Integrated-Predictive-Modeling-Program software) were analyzed by JMP software. Heating mash broiler feed at 75°, 85°, and 95°C decreased (P < 0.05) Salmonella cell counts by >6 log₁₀CFU/g after 180, 60, and 50 s, respectively. Heating E. faecium in feed at 75°, 85°, and 95°C for 180, 120, and 70 s achieved reductions of 3, 6, and >6.5 log₁₀CFU/g, respectively. D-values of linear, Weibull models, and z-value of Salmonella at 75°, 85°, and 95°C were 1.8 to 11.2, 4.2 to 21.8, and 28.6 s, respectively, which were lower (P < 0.05) than those of E. faecium (3.7–18.1, 8.5–34.4, and 34.1 s). Linear with Tail, Linear with Tail and Shoulder, and Weibull with tail equations revealed that E. faecium were more resistant (P < 0.05) to heat than Salmonella as shown by longer “Shoulder-time” (26.5 vs. 16.2 s) and greater “Tail” effect (4.4–4.5 vs. 2.5–2.6 log₁₀CFU/g). Results clearly suggested that E. faecium can be used as a surrogate for Salmonella to validate thermal inactivation during feed manufacture.

There has been extensive interest in the role of serotonin (5-hydoxytryptamine, 5-HT) in the pathogenesis of pulmonary hypertension because episodes of pulmonary arterial hypertension in humans have been linked to serotoninergic appetite-suppressant drugs. In this study, we investigated the role of serotonin in the development of pulmonary hypertension induced by intravenously injecting bacterial lipopolysaccharide (LPS, endotoxin) and cellulose microparticles. In experiment 1, we used a 5-HT ELISA kit for the in vitro quantitative determination of 5-HT in plasma during the development of pulmonary hypertension induced by injecting LPS and cellulose microparticles i.v. in broilers. In experiment 2, broilers were either chronically infused with 5-HT via surgically implanted osmotic pumps or received sham surgery as a control. After a period of 10 d, the pulmonary arterial pressure was recorded during challenge with injected LPS or microparticles. Microparticles elicited 5-HT plasma levels more than 2-fold greater than those elicited by LPS from 15 to 45 min postinjection. This indicates that 5-HT is an important mediator in the pulmonary hypertensive response of broilers to microparticles, but may not play a prominent role in the pulmonary hypertensive response to LPS. Furthermore, chronic 5-HT infusion via osmotic pumps caused an increase in the duration of the pulmonary hypertensive response of broilers to microparticles, indicating that the infused 5-HT was sequestered by circulating thrombocytes and then released upon microparticle-mediated thrombocyte activation. Serotonin appears to play a less prominent role in the pulmonary hypertensive response of broilers to LPS, indicating that other mediators within the innate response to inflammatory stimuli may also be involved. These results are consistent with our hypothesis that pulmonary arterial hypertension ensues when vasoconstrictors such as 5-HT overwhelm the dilatory affects of vasodilators such as nitric oxide, thereby effectively reducing the pulmonary vascular capacity of pulmonary arterial hypertension-susceptible broilers.

Major histocompatibility (B) complex haplotypes B^(Q) and B¹⁷ were examined for their effect on Rous sarcoma outcome. Pedigree matings ofB^QB¹⁷ chickens from the second backcross generation (BC2) of Line UCD 001 (B^(Q)B^(Q)) mated to Line UCD 003 (B¹⁷B¹⁷) produced progeny with genotypes B^(Q)B^(Q), B^QB¹⁷, and B17B17. Six-week-old chickens were injected with subgroup A Rous sarcoma virus (RSV). The tumors were scored for size at 2, 3, 4, 6, 8, and 10 weeks postinoculation. A tumor profile index (TPI) was assigned to each bird based on the six tumor scores. Two experiments with two trials each were conducted. In Experiment 1, chickens (n = 84) were inoculated with 30 pock-forming units (pfu) RSV. There was no significant B genotype effect on tumor growth over time or TPI among the 70 chickens that developed tumors. Chickens (n = 141) were injected with 15 PFU RSV in Experiment 2. The B genotype significantly affected tumor growth pattern over time in the 79 chickens with sarcomas. The B^QB¹⁷ chickens had the lowest TPI, which was significantly different from B17B17 but not B(Q)B(Q). The data indicate complementation because more tumor regression occurs in the B^QB¹⁷ heterozygote than in either B^(Q)B^(Q) or B17B17 genotypes at a 15 pfu RSV dose and significantly so compared to B¹⁷B¹⁷. By contrast, the 30 pfu RSV dose utilized in the first experiment overwhelmed all genotypic combinations of the B^(Q) and B¹⁷ haplotypes, suggesting that certain MHC genotypes affect the immune response under modest levels of viral challenge.

The tightly linked A and E blood alloantigen systems are 2 of 13 blood systems identified in chickens. Reported herein are studies showing that the genes encoding A and E alloantigens map within or near to the chicken regulator of complement activation (RCA) gene cluster, a region syntenic with the human RCA. Genome-wide association studies, sequence analysis, and sequence-derived single-nucleotide polymorphism information for known A and/or E system alleles show that the most likely candidate gene for the A blood system is C4BPM gene (complement component 4 binding protein, membrane). Cosegregation of single-nucleotide polymorphism–defined C4BPM haplotypes and blood system A alleles defined by alloantisera provide a link between chicken blood system A and C4BPM. The best match for the E blood system is the avian equivalent of FCAMR (Fc fragment of IgA and IgM receptor). C4BPM is located within the chicken RCA on chicken microchromosome 26 and is separated from FCAMR by 89 kbp. The genetic variation observed at C4BPM and FCAMR could affect the chicken complement system and differentially guide immune responses to infectious diseases.