Date of Graduation

9-2025

Document Type

Dissertation

Degree Name

Doctor of Philosophy in Biology (PhD)

Degree Level

Graduate

Department

Biological Sciences

Advisor/Mentor

Rhoads, Douglas

Committee Member

Charles Rosenkrans

Third Committee Member

Jingyi Chen

Fourth Committee Member

Navam Hettiarachchy

Keywords

Ascites; BCO; Chicken; Gene expression; Lameness; Mitochondrial Biogenesis

Abstract

Modern broiler production faces persistent challenges from metabolic and skeletal disorders, particularly ascites and bacterial chondronecrosis with osteomyelitis (BCO), which compromise animal welfare and production efficiency. This dissertation examines two key factors that contribute to these conditions: mitochondrial gene expression associated with pulmonary hypertension syndrome (PHS) and the role of intestinal barrier integrity in mitigating lameness. In the first study, the expression of mitochondrial genes COXII and ATP6 was evaluated in the breast, thigh, and lung tissues of three broiler genetic lines—ascites-susceptible (SUS), ascites-resistant (RES), and unselected relaxed (REL). While no significant expression differences were observed in muscle tissues, SUS birds exhibited notably lower COXII expression in the lungs (p = 0.022), with a similar trend in ATP6, indicating a potential link between impaired mitochondrial function and ascites susceptibility. These results suggest that oxygen utilization and mitochondrial adaptation in lung tissue are critical in ascites resistance. In the second study, the efficacy of glycosylated 1,25-dihydroxyvitamin D₃ (G-1,25(OH)₂D₃) as a dietary intervention for BCO lameness was evaluated through its effect on intestinal tight junction gene expression. Cobb 500 broilers were reared on wire and litter flooring, with BCO induced via aerosol exposure carrying pathogenic bacteria from the wire flooring pen, and were assigned to diets containing 0, 0.5, 1.0, or 2.0 µg/kg of G-1,25(OH)₂D₃. The 1.0 µg/kg dose significantly reduced lameness incidence (53.7%; p < 0.001) while enhancing the expression of MUC4, OCLN, and CLDN2 in the jejunum, indicating improved gut barrier function. Although the 2.0 µg/kg dose produced similar gene expression outcomes, the 1.0 µg/kg level was identified as the most cost-effective strategy. Together, these findings contribute to a broader understanding of how mitochondrial function and intestinal health influence broiler resilience to metabolic and skeletal disorders. Targeted genetic selection and nutritional modulation, such as G-1,25(OH)₂D₃ supplementation, offer promising approaches to enhance broiler performance while addressing welfare concerns. Further research is recommended to investigate the long-term physiological effects of these interventions and their role in preventing poultry diseases.

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