Mycobacterial Adhesion: From Hydrophobic to Receptor-Ligand Interactions

Abstract

Adhesion is crucial for the infective lifestyles of bacterial pathogens. Adhesion to non-living surfaces, other microbial cells, and components of the biofilm extracellular matrix are crucial for biofilm formation and integrity, plus adherence to host factors constitutes a first step leading to an infection. Adhesion is, therefore, at the core of pathogens’ ability to contaminate, transmit, establish residency within a host, and cause an infection. Several mycobacterial species cause diseases in humans and animals with diverse clinical manifestations. Mycobacterium tuberculosis, which enters through the respiratory tract, first adheres to alveolar macrophages and epithelial cells leading up to transmigration across the alveolar epithelium and containment within granulomas. Later, when dissemination occurs, the bacilli need to adhere to extracellular matrix components to infect extrapulmonary sites. Mycobacteria causing zoonotic infections and emerging nontuberculous mycobacterial pathogens follow divergent routes of infection that probably require adapted adhesion mechanisms. New evidence also points to the occurrence of mycobacterial biofilms during infection, emphasizing a need to better understand the adhesive factors required for their formation. Herein, we review the literature on tuberculous and nontuberculous mycobacterial adhesion to living and non-living surfaces, to themselves, to host cells, and to components of the extracellular matrix.

Characteristics of clinical isolates of nontuberculous mycobacteria in Java-Indonesia: A multicenter study

“…Infection begins with adhesion to host tissues and cells. The hydrophobicity of the cell wall is a factor that affects the ability to adhere [ 46 ]. The results of this study showed that the number of bacteria capable of adhesion and invasion was higher in the M .…”

Antimycobacterial Activities of Hydroxamic Acids and Their Iron(II/III), Nickel(II), Copper(II) and Zinc(II) Complexes

“…In order to identify whether the HA derivatives have antimycobacterial activities, we assessed these activities in planktonic and stress conditions with high glycerol concentrations leading to biofilm development. Biofilm conditions are indeed known to better mimic stressful in vivo conditions [26][27][28]. These antimycobacterial activities were assessed using three strains, harboring various characteristics, among others, the presence or absence of PDIM lipids in their cell wall: the H37Ra M. tuberculosis strain is PDIM-negative and is a slow-growing strain; the M. marinum is PDIM-positive and a slow-growing mycobacterium (however, in planktonic cultures, it grows faster than M. bovis BCG or H37Ra M. tuberculo-sis strains); and the M. bovis BCG is PDIM-positive and a slow-growing mycobacterium.…”

A Loss of Function in LprG−Rv1410c Homologues Attenuates Growth during Biofilm Formation in Mycobacterium smegmatis

“…Diverse factors drive mycobacterial biofilm formation, as has been reviewed elsewhere [22][23][24] and in detail for multiple mycobacterial species by Chakraborty and Kumar [25]. For the two most highly studied species, M. tuberculosis and M. smegmatis, the most consistent association has been with lipids, including free mycolic acids (FMA) [11,13], mycolyl diacylglycerides (MDAG) [26], monomeromycolyl diacylglycerides (MMDAG) [7,27], mycolate wax esters (MWE) [7,8,27] and, in M. smegmatis, glycopeptidolipids (GPL) [9,28].…”