Abstract
Candida species are commensals but some develop biofilms in prosthetic materials and host surfaces that may represent up to 30% of deaths related to infections, particularly in immunosuppressed patients. Tumor necrosis factor (TNF) exhibits a plethora of functions in host defense mechanisms whereas excessive release of TNF in inflammation promotes tissue damage. Cytokines released in an inflammatory milieu may influence the development of microorganisms either by promoting their growth or displaying antimicrobial activity. In protozoa, TNF may affect growth by coupling through a lectin-like domain, distinct from TNF receptors. TNF was also shown to interact with bacteria via a mechanism that does not involve classical TNF receptors. Using an in vitro C. albicans biofilm model, we show that TNF dose-dependently prevents biofilm development that is blocked by incubating TNF with N,N’-diacetylchitobiose, a major carbohydrate component of C. albicans cell wall. This finding represents a relevant and hitherto unknown mechanism that adds to the understanding of why TNF blockade is associated with opportunistic C. albicans infections.
Highlights
Biofilms are the major state that microorganisms utilize in their struggle to thrive since antimicrobials act against their planktonic, free-floating, state
We investigated whether TNF could alter C. albicans in vitro growth
The present findings, showing an as yet unrecognized mechanism of TNF interference with C. albicans biofilm growth are relevant both as the description of a physiological, TNF receptor independent mechanism of this cytokine in host defense against C. albicans as well as the opening of a potential strategy to prevent in vivo Candida biofilm growth
Summary
Biofilms are the major state that microorganisms utilize in their struggle to thrive since antimicrobials act against their planktonic, free-floating, state. Development of aggregates formed by the microorganism and an extracellular coat of secreted components and even host parts leads to biofilm formation[1]. Organization in biofilms after adherence to those devices offers to microorganisms an alternative to evade host defense. TNF acts on mammalian cells via coupling to specific membrane or soluble receptors, leading to cell activation. Considering that TNF has a major protective role against microorganisms, anti-TNF treatment would render patients prone to develop life-threatening infections[4]. Our data, showing a previously unrecognized TNF interference with C. albicans biofilm formation, unravels a protective role of TNF against systemic, life-threatening opportunistic infections. In addition to the importance in the pathogenesis of Candida infections, this finding does offer an alternative to prevent yeast biofilm formation
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