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Published on: November 6, 2020
Lethal and severe coronary arteritis in DBA/2 mice induced by fungal pathogen, CAWS, Candida albicans water-soluble
Noriko Nagi-Miura1, Toshie Harada, Hiroyasu Shinohara
1Laboratory for Immunopharmacology of Microbial Products, School of Pharmacy, Tokyo University of Pharmacy and Life Science, 1432-1 Horinouchi, Hachioji, Tokyo 192-0392, Japan.
Abstract:
CAWS is a microbial pathogen-associated molecular patterns (PAMPs) produced by Candida albicans. CAWS is a mannoprotein-beta-glucan complex and secreted into the culture supernatant. CAWS has various biological effects, causing acute shock and disrupting vascular permeability. Intraperitoneal administration of CAWS induces coronary arteritis in various strains of inbred mice. The CAWS-induced coronary arteritis is strain-dependent and most severe in DBA/2 mice with a significant number of these animals expiring with cardiomegaly during the observation period. In vivo and in vitro, splenocytes of DBA/2 mice produced various cytokines, such as IL-6, TNF-alpha, and IFN-gamma in response to CAWS. GM-CSF was also produced in response to CAWS. The production of cytokines was significantly enhanced in the presence of recombinant GM-CSF. In contrast, anti-GM-CSF significantly reduced the production of TNF-alpha and IFN-gamma. Augmented production of cytokines in response to CAWS would be a key to the severity of coronary arteritis.
Insights
Candida albicans-secreted antigen (CAWS) triggers severe coronary arteritis in mice, particularly DBA/2 strains. Cytokine production, influenced by GM-CSF, is key to this inflammatory response.
Area of Science:
- Immunology
- Microbiology
- Pathology
Background:
- Candida albicans-secreted antigen (CAWS) is a mannoprotein-beta-glucan complex.
- CAWS is known to induce acute shock and disrupt vascular permeability.
Purpose of the Study:
- To investigate the biological effects of CAWS, specifically its role in inducing coronary arteritis.
- To explore the immunological mechanisms underlying CAWS-induced inflammation, focusing on cytokine production.
Main Methods:
- Intraperitoneal administration of CAWS to various inbred mouse strains.
- In vivo and in vitro analysis of splenocyte cytokine production (IL-6, TNF-alpha, IFN-gamma, GM-CSF).
- Assessment of the impact of recombinant GM-CSF and anti-GM-CSF on cytokine production.
Main Results:
- CAWS induced strain-dependent coronary arteritis, most severe in DBA/2 mice, leading to mortality and cardiomegaly.
- Splenocytes from DBA/2 mice produced IL-6, TNF-alpha, IFN-gamma, and GM-CSF in response to CAWS.
- GM-CSF augmented, while anti-GM-CSF reduced, the production of TNF-alpha and IFN-gamma.
Conclusions:
- CAWS is a potent inducer of coronary arteritis in susceptible mouse strains.
- Augmented cytokine production, modulated by GM-CSF, plays a critical role in the severity of CAWS-induced arteritis.
