Macrophage Migration Is Impaired within Candida albicans Biofilms.

Maria Alonso,Judith Bain,Neil Gow,Lars Erwig

doi:10.3390/jof3030031

Abstract

Candida albicans is an opportunistic fungal pathogen that infects immunocompromised patients. Infection control requires phagocytosis by innate immune cells, including macrophages. Migration towards, and subsequent recognition of, C. albicans fungal cell wall components by macrophages is critical for phagocytosis. Using live-cell imaging of phagocytosis, the macrophage cell line J774.1 showed enhanced movement in response to C. albicans cell wall mutants, particularly during the first 30 min, irrespective of the infection ratio. However, phagocyte migration was reduced up to 2-fold within a C. albicans biofilm compared to planktonic fungal cells. Biofilms formed from C. albicans glycosylation mutant cells also inhibited macrophage migration to a similar extent as wildtype Candida biofilms, suggesting that the physical structure of the biofilm, rather than polysaccharide matrix composition, may hamper phagocyte migration. These data illustrate differential macrophage migratory capacities, dependent upon the form of C. albicans encountered. Impaired migration of macrophages within a C. albicans biofilm may contribute to the recalcitrant nature of clinical infections in which biofilm formation occurs.

Highlights

Human mucosal surfaces are frequently colonised by Candida albicans, host surveillance by host innate defense normally prevents the transition from commensal colonisation to infection [1].Protection against candidiasis relies mainly upon professional phagocytes, including neutrophils and macrophages, whose phagocytic uptake and degradation of the target microbe are critical to the inactivation of fungal particles [2]
Macrophage Migration towards C. albicans Is Not Altered by Multiplicity of Infection
We first characterised in detail the macrophage response to live C. albicans

Summary

Introduction

Human mucosal surfaces are frequently colonised by Candida albicans, host surveillance by host innate defense normally prevents the transition from commensal colonisation to infection [1].Protection against candidiasis relies mainly upon professional phagocytes, including neutrophils and macrophages, whose phagocytic uptake and degradation of the target microbe are critical to the inactivation of fungal particles [2]. Human mucosal surfaces are frequently colonised by Candida albicans, host surveillance by host innate defense normally prevents the transition from commensal colonisation to infection [1]. Fungal growth can occur within a diverse range of host compartments with varying pH and nutrient availabilities, to which this species readily adapts, resulting in multiple C. albicans morphologies that are differentially recognised by immune surveillance mechanisms [3,4,5,6]. Individual yeast cells can initiate biofilm formation on the surfaces of medical and prosthetic devices. Candida biofilms are recalcitrant to antifungal therapy, and can cause prosthetic devices to fail through biofouling of mechanisms. They resist host immune defenses, and are a reservoir from which subsequent infections are disseminated [8]

Methods

Results

Conclusion