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Characterization of cyclophilin 23 as a novel factor for development and pathogenicity of Cryptosporidium parvum

Mengfei Xu1, Xichen Zhang1, Qile Yu1

  • 1State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Key Laboratory for Zoonosis Research of the Ministry of Education, Institute of Zoonosis, and College of Veterinary Medicine, Jilin University, Changchun 130062, China.

Veterinary Parasitology
|July 13, 2025
PubMed

Insights

Cyclophilin 23 (CpCyP23) is crucial for Cryptosporidium parvum development and pathogenicity. Deleting the CpCyP23 gene in C. parvum significantly reduced parasite burden and intestinal damage, suggesting CpCyP23 as a potential therapeutic target.

Area of Science:

  • * Molecular parasitology
  • * Infectious diseases
  • * Protozoology

Background:

  • * Cryptosporidium parvum (C. parvum) is a significant zoonotic protozoan pathogen causing severe diarrhea in humans and animals.
  • * The molecular mechanisms underlying C. parvum pathogenicity are not fully understood.
  • * Nine peptidyl-prolyl cis/trans isomerase (PPIase) genes exist in the C. parvum genome, with potential roles in pathogenicity.

Purpose of the Study:

  • * To investigate the function of cyclophilin 23 (CpCyP23), a PPIase, in C. parvum development and pathogenicity.
  • * To assess the impact of CpCyP23 deletion on C. parvum infection and disease progression.

Main Methods:

  • * CRISPR/Cas9 gene editing was employed to tag and delete the CpCyP23 gene in C. parvum.
  • * Immunofluorescence microscopy was used to determine CpCyP23 expression patterns during parasite development.
  • * In vitro assays using HCT-8 cells and in vivo studies in interferon-γ knockout mice were conducted to evaluate the effects of CpCyP23 deficiency.

Main Results:

  • * CpCyP23 is expressed throughout all critical developmental stages of C. parvum.
  • * Deletion of the CpCyP23 gene led to delayed parasite development in vitro.
  • * Mice infected with C. parvum lacking CpCyP23 showed reduced parasite burden and less small intestinal damage compared to controls.

Conclusions:

  • * CpCyP23 is essential for the normal development of C. parvum.
  • * The absence of CpCyP23 attenuates C. parvum pathogenicity, reducing disease severity.
  • * CpCyP23 represents a promising therapeutic target for controlling cryptosporidiosis.
Keywords:
CRISPR/Cas9Cryptosporidium parvumCyclophilin 23DevelopmentPathogenicity

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