Mechanisms of Pathogenic Candida Species to Evade the Host Complement Attack.

Dhirendra Kumar Singh,Attila Gácser,Renáta Tóth

doi:10.3389/fcimb.2020.00094

Dhirendra Kumar Singh, Attila Gácser + Show 1 more

Open Access

https://doi.org/10.3389/fcimb.2020.00094

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Abstract

Candida species are common colonizers of the human skin, vagina, and the gut. As human commensals, Candida species do not cause any notable damage in healthy individuals; however, in certain conditions they can initiate a wide range of diseases such as chronic disseminated candidiasis, endocarditis, vaginitis, meningitis, and endophthalmitis. The incidence of Candida caused infections has increased worldwide, with mortality rates exceeding 70% in certain patient populations. C. albicans, C. glabrata, C. tropicalis, C. parapsilosis, and C. krusei are responsible for more than 90% of Candida-related infections. Interestingly, the host immune response against these closely related fungi varies. As part of the innate immune system, complement proteins play a crucial role in host defense, protecting the host by lysing pathogens or by increasing their phagocytosis by phagocytes through opsonization. This review summarizes interactions of host complement proteins with pathogenic Candida species, including C. albicans and non-albicans Candida species such as C. parapsilosis. We will also highlight the various ways of complement activation, describe the antifungal effects of complement cascades and explore the mechanisms adopted by members of pathogenic Candida species for evading complement attack.

Highlights

Specialty section: This article was submitted to Fungal Pathogenesis, a section of the journal Frontiers in Cellular and Infection
Increasing incidence of candidemia caused by non- albicans Candida (NAC) species has been reported in the latest decade, that led to the rise of NAC investigations (Andes et al, 2016; Strollo et al, 2016)
In the followings we summarize how various complement proteins shape defense mechanisms to prevent the development of disseminated candidiasis and how such mechanisms could be avoided by Candida species

Summary

Introduction

Specialty section: This article was submitted to Fungal Pathogenesis, a section of the journal Frontiers in Cellular and Infection. The thick cell wall of pathogenic fungi builds a certain level of resistance to direct lysis due to complement activation, binding of complement factors to the fungal surface facilitates their phagocytosis and alters inflammatory responses from host immune cells (Kozel, 1996; Cheng et al, 2012; van Strijp et al, 2015). This revealed that antibodies against complement factor B but not against C1q inhibit the cascade induced by purified chitin, suggesting that mainly the AP is activated by this cell wall component (Roy et al, 2013).

Results

Conclusion