The mucormycete-host interface

Abstract

Mucormycosis is a fungal infection with fulminant angioinvasion leading to high morbidity and mortality in susceptible individuals. The major predisposing conditions are uncontrolled diabetes, neutropenia, malignancies, receipt of a transplant and traumatic injury [1]. Over the past decade, mucormycosis has become an emerging fungal infection due to the increase in patient groups presenting with these pre-disposing conditions and our medical advances in diagnosing the infection [2-4]. Yet, we currently lack clinical interventions to treat mucormycosis effectively. This in turn is due to a lack of understanding of mucormycosis pathogenesis. Here, we discuss our current understanding of selected aspects of interactions at the mucormycete-host interface. We will highlight open questions that might guide future research directions for investigations into the pathogenesis of mucormycosis and potential innovative therapeutic approaches.

Figure 1. Spore germination and filamentous growth of Rhizopus microsporus

Resting spores start to swell shortly after incubation in rich media. First germ tubes are produced after approximately 7 hours incubation with a hyphal network established at 13 hours incubation. Scale bar 50 μm.

Figure 2. Colocalization of host cell GRP78 and R. delemar CotH during invasion of human umbilical vein endothelial cells

GRP78 (green) is labeled with Alexa Fluor 488, CotH (red) is labeled with Alexa Fluor 658. Merged image show colocolization (yellow) of endocytosed fungal swollen spores ∼60 min after incubation. Scale bar 10 μm.

Figure 2. Colocalization of host cell GRP78 and R. delemar CotH during invasion of human umbilical vein endothelial cells

GRP78 (green) is labeled with Alexa Fluor 488, CotH (red) is labeled with Alexa Fluor 658. Merged image show colocolization (yellow) of endocytosed fungal swollen spores ∼60 min after incubation. Scale bar 10 μm.