Neonatal mouse gut metabolites influence cryptosporidium parvum infection in intestinal epithelial cells

Kelli L. Vandussen, Lisa J. Funkhouser-Jones, Marianna E. Akey, Deborah A. Schaefer, Kevin Ackman, Michael W. Riggs, Thaddeus S. Stappenbeck, L. David Sibley

Research output: Contribution to journalArticlepeer-review

16 Scopus citations


The 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.

Original languageEnglish
Article numbere02582-20
Pages (from-to)1-16
Number of pages16
Issue number6
StatePublished - Nov 1 2020


  • 16S rRNA
  • Cryptosporidium parvum
  • Enteric infection
  • Essential nutrient
  • Fatty acid
  • Metabolite
  • Microbiota


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