Trichophyton rubrum LysM proteins bind to fungal cell wall chitin and to the N-linked oligosaccharides present on human skin glycoproteins.

Bibekananda Kar,Stephen J Free,Pavan Patel,Katherine A Borkovich

doi:10.1371/journal.pone.0215034

Bibekananda Kar, Stephen J Free + Show 2 more

Open Access

https://doi.org/10.1371/journal.pone.0215034

Copy DOI

Journal: PloS one	Publication Date: Apr 4, 2019
Citations: 17	License type: CC BY 4.0

Affiliation: University at Buffalo, State University of New York

Abstract

The Trichophyton rubrum genome contains six proteins containing two or more lysin M (LysM) domains. We have characterized two of these proteins, LysM1 and LysM2, and demonstrated that these proteins have the capacity to bind two substrates, chitin and N-linked oligosaccharides associated with human skin glycoproteins. We have characterized the individual LysM domains in LysM1, and shown that the protein contains two functional LysM domains. Each of these domains can bind to chitin, to N-linked oligosaccharides in human skin glycoproteins, and to N-linked oligosaccharides on fungal glycoproteins. We hypothesize that LysM proteins could provide the pathogen with three important functions. First, the T. rubrum LysM proteins could shield host cell wall chitin from the human immune system. Second, the LysM proteins could shield the pathogen’s glycoproteins from host degradation and immune surveillance. Third, the LysM proteins could help facilitate pathogen adhesion to human skin.

Highlights

Human-pathogenic dermatophytes exclusively infect keratinized tissues of human skin, nails, and hair [1]
We demonstrate that LysM1 and LysM2 bind to chitin and that the proteins bind to the N. crassa and T. rubrum cell walls
We hypothesize that the binding is likely to be to the cell wall chitin or glucans based on the fact that lysin M (LysM) domains recognize carbohydrates, and on the results shown in Fig 2B demonstrating that LysM1 binds to the cell wall of the N. crassa Δoch-1 mutant, which is largely devoid of cell wall protein

Summary

Introduction

Human-pathogenic dermatophytes exclusively infect keratinized tissues of human skin, nails, and hair [1]. Unlike fungal infections caused by opportunistic fungi in compromised hosts, the dermatophytes are obligate animal pathogens and infect healthy hosts. Superficial dermatophyte infections are very common, and 10–20% of the worldwide human population suffer from dermatophyte infections [1]. These infections are often very difficult to treat and have a high frequency of reoccurrence [3]. Trichophyton rubrum is the most common fungal dermatophyte and is known to account for 60% of all clinical dermatophyte infections. The fungus causes a variety of chronic skin infections including toenail infections (onychomycosis) athlete’s foot (tinea pedis), ringworm (tinea capitis), and jock itch (tinea cruris)

Methods

Results

Conclusion