ArticleInfection and immunity1994
Cryptosporidium parvum infection of Caco-2 cell monolayers induces an apical monolayer defect, selectively increases transmonolayer permeability, and causes epithelial cell death.
Article in Infection and immunity, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
37 citing papers in PubMed, 116 citations in OpenAlex.
- Convergent mechanisms of epithelial cell structure manipulation by intestinal pathogens.PLoS pathogens · 2025Review
- Article
- Early immune and host cell responses toFrontiers in parasitology · 2023Article
- Cryptosporidium rhoptry effector protein ROP1 injected during invasion targets the host cytoskeletal modulator LMO7.Cell host & microbe · 2021Article
- Changes in the Microbiome ofMicroorganisms · 2020Article
- The transcriptome of Cryptosporidium oocysts and intracellular stages.Scientific reports · 2019Article
- Transcriptome analysis of pig intestinal cell monolayers infected with Cryptosporidium parvum asexual stages.Parasites & vectors · 2018Article
- Drug Development Against the Major Diarrhea-Causing Parasites of the Small Intestine, Cryptosporidium and Giardia.Frontiers in microbiology · 2015Review
- Intra-subtype variation in enteroadhesion accounts for differences in epithelial barrier disruption and is associated with metronidazole resistance in Blastocystis subtype-7.PLoS neglected tropical diseases · 2014Article
- Prospects for immunotherapy and vaccines against Cryptosporidium.Human vaccines & immunotherapeutics · 2014Review
- Effects of the Chinese medicine matrine on experimental C. parvum infection in BALB/c mice and MDBK cells.Parasitology research · 2012Article
- Cell sorting-assisted microarray profiling of host cell response to Cryptosporidium parvum infection.Infection and immunity · 2010Article
- Over-expression and localization of a host protein on the membrane of Cryptosporidium parvum infected epithelial cells.Molecular and biochemical parasitology · 2009Article
- Cryptosporidium parvum DNA replication in cell-free culture.The Journal of parasitology · 2009Article
- Pathophysiology of diarrhea in calves.The Veterinary clinics of North America. Food animal practice · 2009Review
- Cooperative role of macrophages and neutrophils in host Antiprotozoan resistance in mice acutely infected with Cryptosporidium parvum.Infection and immunity · 2008Article
- Detection of epithelial-cell injury, and quantification of infection, in the HCT-8 organoid model of cryptosporidiosis.The Journal of infectious diseases · 2008Article
- Calpain regulates enterocyte brush border actin assembly and pathogenic Escherichia coli-mediated effacement.The Journal of biological chemistry · 2003Article
- Purification of Sarcocystis neurona sporocysts from opossum (Didelphis virginiana) using potassium bromide discontinuous density gradient centrifugation.Parasitology research · 2003Article
- In vitro cultivation of cryptosporidium species.Clinical microbiology reviews · 2002Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Caco-2 cells were grown on permeable filters and infected with Cryptosporidium parvum. Infection rates exceeded 50% of target cells with a sufficient inoculum dose of parasites. Infection induced a dose- and time-dependent fall in transmonolayer resistance, which was closely related to both the inoculum dose and the number of parasites detected by immunofluorescence. Caco-2a, MDBK, and MDBK subclone F5D2 evidenced similar declines in resistance when grown and infected under similar circumstances. Caco-2 monolayers became permeable to molecules of < or = 1,000 Da but continued to remain impermeable to exogenously added, or endogenously produced, proteins of > or = 1,881 Da. We found that infected monolayers released up to 50% of the total cellular lactase dehydrogenase into apical media, but not basal media, and that the vital dye propidium iodide avidly stained infected cells, and often parasites, when added to the apical reservoir. Cryptosporidium infection of Caco-2 monolayers increases transmonolayer permeability, induces an apical cellular and monolayer defect, and causes cell death.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.