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Investigation of OCH1 in the Virulence of Candida parapsilosis Using a New Neonatal Mouse Model
Katalin Csonka1, Máté Vadovics1, Annamária Marton2
1Department of Microbiology, University of SzegedSzeged, Hungary.
Insights
A new intravenous neonatal mouse model effectively studies Candida parapsilosis infections in newborns. This model revealed strain-specific differences and the role of OCH1 in fungal pathogenicity and immune response.
Area of Science:
- Mycology
- Infectious Diseases
- Neonatal Research
Background:
- Candida parapsilosis is a significant threat to neonates, especially premature infants in ICUs.
- Existing in vivo models for systemic candidiasis in newborns are limited, with many using less efficient infection routes.
- Understanding neonatal immune responses to Candida infections is crucial for effective treatment.
Purpose of the Study:
- To establish a novel intravenous neonatal mouse model for studying systemic Candida parapsilosis infection.
- To analyze the pathogenic properties of different C. parapsilosis strains using this model.
- To investigate the role of the OCH1 gene in C. parapsilosis virulence and host immune response in neonates.
Main Methods:
- Development of an intravenous infection model in 2-day-old BALB/c mouse pups via the external facial vein.
- Infection with different doses of C. parapsilosis strains, including wild-type and an OCH1 mutant.
- Assessment of fungal dissemination through organ colonization (spleen, kidney, liver, brain) and histological examination.
- Measurement of cytokine (TNFα, KC, IL-1β) expression levels in infected neonatal mice.
Main Results:
- The novel intravenous model demonstrated homogenous dissemination of C. parapsilosis in neonatal organs.
- Significant differences in fungal burden were observed between C. parapsilosis CLIB and GA1 strains.
- The C. parapsilosis OCH1 mutant showed attenuated virulence compared to the wild-type strain in neonatal mice.
- Infection led to elevated levels of TNFα, KC, and IL-1β, with higher expression in response to the OCH1 mutant.
Conclusions:
- The developed intravenous neonatal mouse model is effective for studying systemic C. parapsilosis infection.
- The OCH1 gene plays a significant role in C. parapsilosis pathogenicity and influences the host's inflammatory cytokine response.
- This model provides a valuable tool for future research on neonatal candidiasis and antifungal strategies.
Abstract:
Candida parapsilosis is an opportunistic human fungal pathogen that poses a serious threat to low birth weight neonates, particularly at intensive care units. In premature infants, the distinct immune responses to Candida infections are not well understood. Although several in vivo models exist to study systemic candidiasis, only a few are available to investigate dissemination in newborns. In addition, the majority of related studies apply intraperitoneal infection rather than intravenous inoculation of murine infants that may be less efficient when studying systemic invasion. In this study, we describe a novel and conveniently applicable intravenous neonatal mouse model to monitor systemic C. parapsilosis infection. Using the currently developed model, we aimed to analyze the pathogenic properties of different C. parapsilosis strains. We infected 2 days-old BALB/c mouse pups via the external facial vein with different doses of C. parapsilosis strains. Homogenous dissemination of yeast cells was found in the spleen, kidney, liver and brain of infected newborn mice. Colonization of harvested organs was also confirmed by histological examinations. Fungal burdens in newborn mice showed a difference for two isolates of C. parapsilosis. C. parapsilosis CLIB infection resulted in higher colonization of the spleen, kidney and liver of neonatal mice compared to the C. parapsilosis GA1 strain at day 2 after the infection. In a comprehensive study with the adult mice infection, we also presented the attenuated virulence of a C. parapsilosis cell wall mutant (OCH1) in this model. Significantly less och1Δ/Δ null mutant cells were recovered from the spleen, kidney and liver of newborn mice compared to the wild type strain. When investigating the cytokine response of neonatal mice to C. parapsilosis infection, we found elevated TNFα, KC, and IL-1β expression levels in all organs examined when compared to the uninfected control. Furthermore, all three measured cytokines showed a significantly elevated expression when newborn mice were infected with och1Δ/Δ cells compared to the wild type strain. This result further supported the inclusion of OCH1 in C. parapsilosis pathogenicity. To our current knowledge, this is the first study that uses a mice neonatal intravenous infection model to investigate C. parapsilosis infection.
