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Candidiasis--do we need to fight or to tolerate the Candida fungus?
M Raska1, J Bĕláková, M Krupka
1Department of Immunology, Medical Faculty, Palacký University, 772 00 Olomouc, Czechia. raskamil@uab.edu
Abstract:
Candidiases, infections caused by germination forms of the Candida fungus, represent a heterogeneous group of diseases from systemic infection, through mucocutaneous form, to vulvovaginal form. Although caused by one organism, each form is controlled by distinct host immune mechanisms. Phagocytosis by polymorphonuclears and macrophages is generally accepted as the host immune mechanism for Candida elimination. Phagocytes require proinflammatory cytokine stimulation which could be harmful and must be regulated during the course of infection by the activity of CD8+ and CD4+ T cells. In the vaginal tissue the phagocytes are inefficient and inflammation is generally an unwanted reaction because it could damage mucosal tissue and break the tolerance to common vagina antigens including the otherwise saprophyting Candida yeast. Recurrent form of vulvovaginal candidiasis is probably associated with breaking of such tolerance. Beside the phagocytosis, specific antibodies, complement, and mucosal epithelial cell comprise Candida eliminating immune mechanisms. They are regulated by CD4+ and CD8+ T cells which produce cytokines IL-12, IFN-gamma, IL-10, TGF-beta, etc. as the response to signals from dendritic cells specialized to sense actual Candida morphotypes. During the course of Candida infection proinflammatory signals (if initially necessary) are replaced successively by antiinflammatory signals. This balance is absolutely distinct during each candidiasis form and it is crucial to describe and understand the basic principles before designing new therapeutic and/or preventive approaches.
Insights
Candida infections involve complex immune responses, varying by infection type. Understanding the balance between pro- and anti-inflammatory signals is crucial for developing new treatments for candidiasis.
Area of Science:
- Immunology
- Mycology
- Infectious Diseases
Background:
- Candidiasis encompasses diverse infections caused by Candida fungi, ranging from systemic to mucocutaneous and vulvovaginal forms.
- Distinct host immune mechanisms govern each form, with phagocytosis by immune cells being a primary elimination strategy.
- Inflammation in vaginal tissue can be detrimental, potentially disrupting tolerance to Candida and leading to recurrent infections.
Purpose of the Study:
- To elucidate the distinct immune mechanisms underlying different forms of candidiasis.
- To understand the role of T cells (CD4+ and CD8+) and cytokines in regulating Candida infections.
- To highlight the importance of the pro-inflammatory to anti-inflammatory signal balance in infection control.
Main Methods:
- Review of existing literature on host immune responses to Candida.
- Analysis of the roles of phagocytes, T cells, cytokines (IL-12, IFN-gamma, IL-10, TGF-beta), and dendritic cells.
- Examination of immune regulation in different candidiasis forms, including vulvovaginal candidiasis.
Main Results:
- Phagocytosis requires pro-inflammatory cytokine stimulation, regulated by CD4+ and CD8+ T cells.
- Vaginal immunity presents unique challenges due to inefficient phagocytes and the risk of breaking tolerance.
- Immune responses shift from pro-inflammatory to anti-inflammatory signals during infection, with distinct balances for each candidiasis form.
Conclusions:
- The immune response to Candida is highly context-dependent, varying significantly across different infection types.
- Recurrent vulvovaginal candidiasis may result from a breakdown in immune tolerance.
- A comprehensive understanding of these immune dynamics is essential for advancing therapeutic and preventive strategies against candidiasis.
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