Authors:

Victoria Karaluz

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Cryptosporidium parvum (C. parvum) is a eukaryotic single-celled enteric pathogen that causes intestinal inflammation and diarrhea and can cause potentially life-threatening disease in immunocompromised individuals. C. parvum enters the intestinal tract by ingestion and is activated by bile acids or other compounds in the stomach of the host, allowing the parasite to invade intestinal epithelial cells (IECs). Interferons (IFN) are cytokines produced by IECs as the main defense against viruses and other pathogens. IFNs are produced in response to the detection of a pathogen and upon secretion and binding to their receptor, IFNs facilitate the expression of IFN stimulated genes (ISGs) that are key to the cellular defense against pathogens. Not much is known about the specific IFN response to C. parvum infection and current reports have had contradicting results. This project aims to further understand the complicated interactions between host cell IFN and C. parvum infection susceptibility. C. parvum replication in IECs was measured using qRT-PCT in IFN KO cell lines, IFN receptor KO cell lines, and IFN treated cells. We found that C. parvum infection of T84 IECs induces production of IFNL2/3, but not IFNL1 or IFNB1. Similarly, cells lacking IFNL2/3 displayed an increased replication of C. parvum. However, IFNL2/3 pretreatment of wild type cells did not reduce infection burden, while IFNB1 pretreatment leads to an increase in C. parvum replication. These results point to an anti-infection role of IFNL2/3 and pro-infection role of IFNB1 in C. parvum infection. We aim to further investigate the mechanism by which different types of IFN interact with C. parvum to either promote or defend against infection. This research provides a broader understanding of the complex interactions between IFNs and eukaryotic enteric pathogens within the diverse microbiome of the gut. Investigating the Relationship between

Source:

University of Florida / Victoria Karaluz, Zina M. Uckeleley, Josmar Polanco, / 2023

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Co-authors:

Victoria Karaluz