Abstract
Mycobacterium ulcerans is the causative agent of the chronic, necrotizing skin disease Buruli ulcer. Modes of transmission and molecular mechanisms involved in the establishment of M. ulcerans infections are poorly understood. Interactions with host glycans are often crucial in bacterial pathogenesis and the 22 kDa M. ulcerans protein MUL_3720 has a putative role in host cell attachment. It has a predicted N-terminal lectin domain and a C-terminal peptidoglycan-binding domain and is highly expressed on the surface of the bacilli. Here we report the glycan-binding repertoire of whole, fixed M. ulcerans bacteria and of purified, recombinant MUL_3720. On an array comprising 368 diverse biologically relevant glycan structures, M. ulcerans cells showed binding to 64 glycan structures, representing several distinct classes of glycans, including sulfated structures. MUL_3720 bound only to glycans containing sulfated galactose and GalNAc, such as glycans known to be associated with keratins isolated from human skin. Surface plasmon resonance studies demonstrated that both whole, fixed M. ulcerans cells and MUL_3720 show high affinity interactions with both glycans and human skin keratin extracts. This MUL_3720-mediated interaction with glycans associated with human skin keratin may contribute to the pathobiology of Buruli ulcer.
Highlights
Buruli ulcer (BU) is a chronic, necrotizing skin disease, caused by Mycobacterium ulcerans [1]
Mycobacterium ulcerans causes a skin-based disease known as Buruli ulcer
The only well characterized bacterial factor in Buruli ulcer pathogenesis is mycolactone, a toxin produced by the bacteria
Summary
Buruli ulcer (BU) is a chronic, necrotizing skin disease, caused by Mycobacterium ulcerans [1]. It affects populations living in contact with stagnant or slow flowing water bodies primarily in West and Central Africa, but has been reported from Asia, the Americas, Papua New Guinea and Australia [2]. In advanced BU lesions, extracellular clusters [6] of the pathogen are residing in completely necrotic areas, primarily localized in deeper layers of subcutaneous fat tissue [7]. Clustering of the bacteria and skin location appear key elements in the long-term persistence of M. ulcerans in the chronically infected immunocompetent host
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