ArticleInfection and immunity2004
Apical organelle discharge by Cryptosporidium parvum is temperature, cytoskeleton, and intracellular calcium dependent and required for host cell invasion.
Article in Infection and immunity, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 88 citations in OpenAlex.
- Highly divergent apicomplexan cytoskeletons provide additional models for actin biology.The FEBS journal · 2025Review
- Cryptosporidium parvum multidrug resistance protein confers resistance to toxic gut microbial metabolite.Cell host & microbe · 2025Article
- CRISPR-based functional profiling of the Toxoplasma gondii genome during acute murine infection.Nature microbiology · 2024Article
- UnveilingFrontiers in cellular and infection microbiology · 2024Article
- Structure-activity relationship of BMS906024 derivatives for Cryptosporidium parvum growth inhibition.Bioorganic & medicinal chemistry letters · 2023Article
- A genetic screen identifies a protective type III interferon response to Cryptosporidium that requires TLR3 dependent recognition.PLoS pathogens · 2022Article
- Protein Kinase C-α Is a Gatekeeper ofInfection and immunity · 2022Article
- Cryptosporidium rhoptry effector protein ROP1 injected during invasion targets the host cytoskeletal modulator LMO7.Cell host & microbe · 2021Article
- Identification and characterization of a new 34 kDa MORN motif-containing sporozoite surface-exposed protein, Cp-P34, unique to Cryptosporidium.International journal for parasitology · 2021Article
- Article
- Monoclonal Antibodies to Intracellular Stages of Cryptosporidium parvum Define Life Cycle ProgressionmSphere · 2018Article
- Delivery of parasite Cdg7_Flc_0990 RNA transcript into intestinal epithelial cells during Cryptosporidium parvum infection suppresses host cell gene transcription through epigenetic mechanisms.Cellular microbiology · 2017Article
- 5-Aminopyrazole-4-Carboxamide-Based Compounds Prevent the Growth of Cryptosporidium parvum.Antimicrobial agents and chemotherapy · 2017Article
- Delivery of Parasite RNA Transcripts Into Infected Epithelial Cells During Cryptosporidium Infection and Its Potential Impact on Host Gene Transcription.The Journal of infectious diseases · 2017Article
- Inhibition of Calcium-Dependent Protein Kinase 1 (CDPK1) In Vitro by Pyrazolopyrimidine Derivatives Does Not Correlate with Sensitivity of Cryptosporidium parvum Growth in Cell Culture.Antimicrobial agents and chemotherapy · 2016Article
- SAR Studies of 5-Aminopyrazole-4-carboxamide Analogues as Potent and Selective Inhibitors ofACS medicinal chemistry letters · 2015Article
- CDPKs of Cryptosporidium parvum--stage-specific expression in vitro.Parasitology research · 2014Article
- Plasmodium berghei calcium dependent protein kinase 1 is not required for host cell invasion.PloS one · 2013Article
- Cryptosporidium pathogenicity and virulence.Clinical microbiology reviews · 2013Review
- Multiple determinants for selective inhibition of apicomplexan calcium-dependent protein kinase CDPK1.Journal of medicinal chemistry · 2012Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
Abstract
The apical organelles in apicomplexan parasites are characteristic secretory vesicles containing complex mixtures of molecules. While apical organelle discharge has been demonstrated to be involved in the cellular invasion of some apicomplexan parasites, including Toxoplasma gondii and Plasmodium spp., the mechanisms of apical organelle discharge by Cryptosporidium parvum sporozoites and its role in host cell invasion are unclear. Here we show that the discharge of C. parvum apical organelles occurs in a temperature-dependent fashion. The inhibition of parasite actin and tubulin polymerization by cytochalasin D and colchicines, respectively, inhibited parasite apical organelle discharge. Chelation of the parasite's intracellular calcium also inhibited apical organelle discharge, and this process was partially reversed by raising the intracellular calcium concentration by use of the ionophore A23187. The inhibition of parasite cytoskeleton polymerization by cytochalasin D and colchicine and the depletion of intracellular calcium also decreased the gliding motility of C. parvum sporozoites. Importantly, the inhibition of apical organelle discharge by C. parvum sporozoites blocked parasite invasion of, but not attachment to, host cells (i.e., cultured human cholangiocytes). Moreover, the translocation of a parasite protein, CP2, to the host cell membrane at the region of the host cell-parasite interface was detected; an antibody to CP2 decreased the C. parvum invasion of cholangiocytes. These data demonstrate that the discharge of C. parvum sporozoite apical organelle contents occurs and that it is temperature, intracellular calcium, and cytoskeleton dependent and required for host cell invasion, confirming that apical organelles play a central role in C. parvum entry into host cells.
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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.