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Expression of Human CEACAM Receptors Promotes Inflammation and Organ Damage During Systemic Candida albicans
Esther Klaile1,2, Mario Marco Müller2,3, Johannes Sonnberger2,4
1Center for Clinical Studies, Jena University Hospital, 07747 Jena, Germany.
Abstract:
Invasive candidiasis is a fungal infection characterized by a high mortality rate. Carcinoembryonic antigen-related cell adhesion molecule (CEACAM) family receptors play a crucial role in regulating innate responses of both leukocytes and epithelia. Human CEACAM3, CEACAM5 and CEACAM6 receptors recognize Candida albicans and are expressed in transgenic CEABAC10 mice. In a murine C. albicans infection model, CEABAC10 mice exhibited a shortened survival period attributed to an early cytokine storm, an exacerbated acute phase response, and heightened systemic inflammation compared to their wild-type littermates. The livers and kidneys of CEABAC10 mice displayed intensified purulent necrotizing inflammation, accompanied by increased infiltration of neutrophils and macrophages. Our in vivo and in vitro data indicated that the expression of CEACAM6 on monocytes of CEABAC10 mice caused the elevated cytokine levels and the subsequent exacerbation of the acute phase response upon C. albicans infection, resulting in decreased survival.
Insights
Transgenic mice expressing human carcinoembryonic antigen-related cell adhesion molecule 3, 5, and 6 (CEACAM3/5/6) showed reduced survival during Candida albicans infection due to heightened inflammation.
Area of Science:
- Immunology
- Mycology
- Cell Biology
Background:
- Invasive candidiasis is a severe fungal infection with high mortality.
- Carcinoembryonic antigen-related cell adhesion molecule (CEACAM) receptors regulate innate immune responses.
- Human CEACAM3, CEACAM5, and CEACAM6 recognize Candida albicans.
Purpose of the Study:
- To investigate the role of CEACAM receptors in a murine model of invasive candidiasis.
- To determine the impact of CEACAM expression on immune response and survival during Candida albicans infection.
Main Methods:
- Utilized transgenic CEABAC10 mice expressing human CEACAM3, CEACAM5, and CEACAM6.
- Inoculated mice with Candida albicans to establish a murine infection model.
- Analyzed survival rates, cytokine levels, acute phase response, and inflammatory markers in livers and kidneys.
Main Results:
- CEABAC10 mice exhibited significantly shortened survival compared to wild-type littermates.
- CEABAC10 mice developed an early cytokine storm, exacerbated acute phase response, and heightened systemic inflammation.
- Intensified necrotizing inflammation and increased neutrophil/macrophage infiltration were observed in CEABAC10 mouse livers and kidneys.
- CEACAM6 expression on monocytes was identified as a key factor in elevated cytokine levels and exacerbated inflammation.
Conclusions:
- CEACAM receptor expression, particularly CEACAM6 on monocytes, exacerbates the immune response to Candida albicans infection.
- This heightened inflammatory response leads to decreased survival in CEABAC10 mice.
- CEACAMs represent potential therapeutic targets for managing invasive candidiasis.
