Date of Defense
5-6-2026 9:00 AM
Location
F3-136
Document Type
Thesis Defense
Degree Name
Master of Science in Molecular Biology and Biotechnology
College
COS
Department
Biology
First Advisor
Dr. Khalid Muhammad
Keywords
Allergic contact dermatitis, contact hypersensitivity, gut microbiota, cytokines, inflammation, T cells, kinetin, dysbiosis
Abstract
Allergic contact dermatitis is T cell mediated inflammatory skin disorder commonly studied using contact hypersensitivity mouse model. It induces local inflammation and further evidence suggests that gut microbiome also contributes to disease progression. However, kinetin, a natural plant hormone modulates these immune processes. After TNCB successfully induces CHS, kinetin treatment resulted in significant reduction in serum IgE levels while its effect on ear swelling and histological changes were modest. Microbiome analysis revealed no major difference in alpha diversity instead beta diversity demonstrated increased microbial heterogeneity in TNCB-treated mice group. Conversely, Kinetin-treated groups exhibited a microbial profile similar to wild type group which suggested partial preservation of microbiome stability. Genus level and Random Forest analysis further implied that TNCB was associated with shifts in specific microbial taxa connected to inflammation, while kinetin treatment was linked to moderate compositional changes. These findings indicate that kinetin does not completely suppress CHS but may exert modest immunomodulatory effect and help to limit microbiome disruption. Overall, this study provides insight upon the interplay between inflammation, gut microbiota and CHS. It also suggests that kinetin may have a potential modulatory effect on both systemic immune responses and microbial balance.
Included in
EXPLORING THE THERAPEUTIC POTENTIAL OF KINETIN IN ALLERGIC CONTACT DERMATITIS
F3-136
Allergic contact dermatitis is T cell mediated inflammatory skin disorder commonly studied using contact hypersensitivity mouse model. It induces local inflammation and further evidence suggests that gut microbiome also contributes to disease progression. However, kinetin, a natural plant hormone modulates these immune processes. After TNCB successfully induces CHS, kinetin treatment resulted in significant reduction in serum IgE levels while its effect on ear swelling and histological changes were modest. Microbiome analysis revealed no major difference in alpha diversity instead beta diversity demonstrated increased microbial heterogeneity in TNCB-treated mice group. Conversely, Kinetin-treated groups exhibited a microbial profile similar to wild type group which suggested partial preservation of microbiome stability. Genus level and Random Forest analysis further implied that TNCB was associated with shifts in specific microbial taxa connected to inflammation, while kinetin treatment was linked to moderate compositional changes. These findings indicate that kinetin does not completely suppress CHS but may exert modest immunomodulatory effect and help to limit microbiome disruption. Overall, this study provides insight upon the interplay between inflammation, gut microbiota and CHS. It also suggests that kinetin may have a potential modulatory effect on both systemic immune responses and microbial balance.