ORCID

https://orcid.org/0009-0003-6048-9987

Keywords

Inflammatory Bowel Disease(IBD), Dextran Sodium Sulfate(DSS), Caco-2 cells, Intestinal epithelial barrier, IL-6 signaling, Microbial metabolites

Subject Categories

Cell Biology | Digestive System Diseases

Abstract

Dextran sodium sulphate (DSS) is widely used in vivo to induce epithelial injury; however, the molecular effects of DSS on intestinal epithelial cells, that investigate inflammatory and metabolic repair mechanisms remain unclear. Here, we establish an in vitro DSS-induced epithelial damage model using differentiated Caco-2 cell monolayer. Exposure to 2.5%(w/v) DSS for 24 hours resulted in significant upregulation of pore forming protein Claudin-2(2.677-fold) and oxidative marker, NOX-1(1.866-fold), accompanied by increased ROS production confirmed via DHE staining. Increased epithelial permeability was observed by TEER analysis, without significant cytotoxicity. Surprisingly, ELISA analysis revealed significant downregulation of IL-6 (p-value< 0.0073). We recently reported the protective effects of butyric acid and low dose of rIL-6 in the intestinal epithelium. Hence, treatment of low to moderate IL-6 doses (0.5-1ng/ml) promoted barrier repair, whereas higher doses(5ng/ml) induced barrier damage, as confirmed by Western blot and immunocytochemistry. Furthermore, treatment of DSS-damaged Caco-2 monolayer with 10 mM butyric acid significantly enhanced epithelial healing. Collectively, this study establishes a robust DSS-induced colitis model and highlights the therapeutic potential of use of butyric acid and low dose of rIL-6 for treatment of Crohn’s disease and ulcerative colitis.

Keywords: Dextran Sodium Sulfate (DSS), Inflammatory Bowel Disease (IBD), IL-6, Caco-2, Cytokines, Epithelial Barrier, Butyric acid

Completion Date

2026

Semester

Summer

Committee Chair

Saleh Naser

Degree

Master of Science (M.S.)

College

College of Medicine

Department

Burnett School of Biomedical Sciences

Format

PDF

Document Type

Thesis

Language

English

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