Document Type

Honors Project

Publication Date

6-11-2026

Abstract

Schistosomiasis is a parasitic disease in humans caused by parasitic flatworms such as Schistosoma mansoni and conservatively kills over 11,000 people per year. The infection is transmitted through freshwater snails like Biomphalaria glabrata in waters contaminated with mammalian feces. The cercarial form of the worm penetrates the skin of mammals and, in late stages of infection, lays eggs in the digestive tract, liver and blood vessels, causing intestinal schistosomiasis. When the immune system of vertebrates senses pathogens, immune cells release pro-inflammatory cytokines. However, the immune system of invertebrates is not nearly as understood. Recent genome advances (Castillo et al, 2020) have identified cytokine sequences in B. glabrata. Two of these cytokines are TNFs and IL-17s, which are regulated by the NF-kB pathway in vertebrates. This study examines the phylogeny of IL-17 and TNF and looks for potential NF-kB binding sites upstream of these cytokines.  This study also focuses on the impacts of Schistosoma mansoni infection on IL-17 and TNF expression in Biomphalaria glabrata and compares B. glabrata susceptible to the infection (NMRI) and non-susceptible B. glabrata (BS90). It was hypothesized that IL-17 and TNF expression levels would change in response to infection and that expression levels would be different between NMRI and BS90 B. glabrata. RT-qPCR results showed a low expression of a TNF sequence and inconclusive expression of an IL-17 sequence in B. glabrata. Further optimization and continued study are required to verify these results.

Level of Honors

magna cum laude

Department

Biology

Advisor

Judith Humphries

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