Neutrophil-Driven Anti-TNFα Resistance in IBD
Session Number
2
Advisor(s)
Dr. Ronen Sumagin, Feinberg School of Medicine
Location
B115
Discipline
Medical and Health Sciences
Start Date
15-4-2026 11:10 AM
End Date
15-4-2026 11:55 AM
Abstract
Inflammatory Bowel Disease (IBD), including Crohn’s Disease and Ulcerative Colitis, is characterized by chronic intestinal inflammation. Although anti-TNFα therapy is commonly used to treat patients who do not respond to standard treatments, up to 40% of patients fail to benefit from this therapy. One potential factor contributing to this resistance is the accumulation of neutrophils in the inflamed mucosa, a type of immune cell involved in inflammatory responses. In this project, neutrophil presence in colon tissue was analyzed in a murine model of anti-TNFα treatment resistance that has been developed in the lab. My role focused on quantifying neutrophil levels in IL10 knockout (IL10KO) mice, with and without epithelial chemical injury inducer Dextran Sodium Sulfate (DSS), modeling inflammatory disease resistant to therapy following anti-TNFα treatment, and comparing to wild-type(WT) mice. Quantification of the neutrophil burden was used as a key scoring parameter that helped determine response to anti-TNFα therapy. Results showed that anti-TNFα treatment decreased neutrophil levels in WT mice but not in IL10KO mice, where inflammation and neutrophil accumulation persisted. This data supports the validity of this new model and the hypothesis that neutrophils contribute to resistance to anti-TNFα therapy in IBD, identifying them as potential therapeutic targets.
Neutrophil-Driven Anti-TNFα Resistance in IBD
B115
Inflammatory Bowel Disease (IBD), including Crohn’s Disease and Ulcerative Colitis, is characterized by chronic intestinal inflammation. Although anti-TNFα therapy is commonly used to treat patients who do not respond to standard treatments, up to 40% of patients fail to benefit from this therapy. One potential factor contributing to this resistance is the accumulation of neutrophils in the inflamed mucosa, a type of immune cell involved in inflammatory responses. In this project, neutrophil presence in colon tissue was analyzed in a murine model of anti-TNFα treatment resistance that has been developed in the lab. My role focused on quantifying neutrophil levels in IL10 knockout (IL10KO) mice, with and without epithelial chemical injury inducer Dextran Sodium Sulfate (DSS), modeling inflammatory disease resistant to therapy following anti-TNFα treatment, and comparing to wild-type(WT) mice. Quantification of the neutrophil burden was used as a key scoring parameter that helped determine response to anti-TNFα therapy. Results showed that anti-TNFα treatment decreased neutrophil levels in WT mice but not in IL10KO mice, where inflammation and neutrophil accumulation persisted. This data supports the validity of this new model and the hypothesis that neutrophils contribute to resistance to anti-TNFα therapy in IBD, identifying them as potential therapeutic targets.