Neonatal mouse gut metabolites influence cryptosporidium parvum infection in intestinal epithelial cells
David, Sibley, L.
AffiliationSchool of Animal and Comparative Biomedical Sciences, College of Agriculture and Life Sciences, University of Arizona
MetadataShow full item record
PublisherAmerican Society for Microbiology
CitationVanDussen KL, Funkhouser-Jones LJ, Akey ME, Schaefer DA, Ackman K, Riggs MW, Stappenbeck TS, Sibley LD. 2020. Neonatal mouse gut metabolites influence Cryptosporidium parvum infection in intestinal epithelial cells. mBio 11:e02582-20.
RightsCopyright © 2020 VanDussen et al. This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International license.
Collection InformationThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at firstname.lastname@example.org.
AbstractThe protozoan parasite Cryptosporidium sp. is a leading cause of diarrheal disease in those with compromised or underdeveloped immune systems, par-ticularly infants and toddlers in resource-poor localities. As an enteric pathogen, Cryptosporidium sp. invades the apical surface of intestinal epithelial cells, where it resides in close proximity to metabolites in the intestinal lumen. However, the effect of gut metabolites on susceptibility to Cryptosporidium infection remains largely unstudied. Here, we first identified which gut metabolites are prevalent in neonatal mice when they are most susceptible to Cryptosporidium parvum infection and then tested the isolated effects of these metabolites on C. parvum invasion and growth in intestinal epithelial cells. Our findings demonstrate that medium or long-chain satu-rated fatty acids inhibit C. parvum growth, perhaps by negatively affecting the stream-lined metabolism in C. parvum, which is unable to synthesize fatty acids. Conversely, long-chain unsaturated fatty acids enhanced C. parvum invasion, possibly by modulat-ing membrane fluidity. Hence, gut metabolites, either from diet or produced by the microbiota, influence C. parvum growth in vitro and may also contribute to the early susceptibility to cryptosporidiosis seen in young animals. © 2020 VanDussen et al.
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Except where otherwise noted, this item's license is described as Copyright © 2020 VanDussen et al. This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International license.
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