ArticleCell host & microbe2025
Cryptosporidium parvum multidrug resistance protein confers resistance to toxic gut microbial metabolite.
Article in Cell host & microbe, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed.
- Genomic heterogeneity of NAD(P)H dehydrogenase predisposes Cryptosporidium to clofazimine resistance.Nature microbiology · 2026Article
- Cryptosporidium secreted proteins form a complex layered interface with the host cell.PLoS pathogens · 2026Article
- Insights into the lifecycle of Cryptosporidium and compounds targeting developmental stages.Current opinion in microbiology · 2026Review
- Gut microbiota modulation in the prevention and treatment of heat stroke.Frontiers in immunology · 2026Review
- New Cryptosporidium parvum fitness factor.Nature reviews. Microbiology · 2025Article
- Widespread genomic heterogeneity at the type II NAD(P)H dehydrogenase locus predisposesbioRxiv : the preprint server for biology · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Cryptosporidium parvum subtypes differ in pathogenicity, but the underlying factors are largely unknown. We show that two genetically similar C. parvum isolates grow equally well in vitro but differ in pathogenicity in immunocompromised mice. Reduced oocyst shedding of the avirulent strain was restored by antibiotic treatment, suggesting susceptibility to colonization resistance imparted by the microbiota. This resistance was associated with a gene encoding a parasite ABC transporter and enhanced infectivity. Molecular analyses indicate that the ABC transporter belongs to a multidrug resistance protein (MRP) family. CpMRP1 binds bacterial metabolites, notably deoxycholic acid (DCA) that inhibits C. parvum growth. CpMRP1 is exported from small granules to the parasite-host interface, potentially mediating the export of xenobiotics. Loss of CpMRP1 reduces infectivity and DCA resistance in mice, and CpMRP1 polymorphisms across isolates determine susceptibility to DCA. These results define CpMRP1 as a determinant of C. parvum sensitivity to microbiome-mediated inhibition, thereby influencing infectivity.
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Registered trials
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