Mycobacterium tuberculosis curli pili (MTP) deficiency is associated with alterations in cell wall biogenesis, fatty acid metabolism and amino acid synthesis

Ashokcoomar, Shinese; Reedoy, K S; Senzani, Sibusiso; Loots, Du Toit; Beukes, Derylize; Reenen, Mari van; Pillay, Balakrishna; Pillay, Manormoney

doi:10.1007/s11306-020-01720-z

Cited by 6 publications

(2 citation statements)

References 72 publications

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“…Recently, Mtb curli pili (MTP) deficiency were found to be associated with alterations in cell wall biogenesis, fatty acid metabolism and amino acid synthesis ( Ashokcoomar et al, 2020 ). Using untargeted GCxGC-MS, 28, 10, and 16 biologically significant differential metabolites were found between the mtp gene-knockout (∆ mtp ) mutants and the wild type (WT), between WT and mtp- complement, and between ∆ mtp to mtp- complemented strains, respectively.…”

Section: Pathogen-based Biomarkersmentioning

confidence: 99%

Biomarker discovery for tuberculosis using metabolomics

Jiang

2023

Front. Mol. Biosci.

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Tuberculosis (TB) is the leading cause of death among infectious diseases, and the ratio of cases in which its pathogen Mycobacterium tuberculosis (Mtb) is drug resistant has been increasing worldwide, whereas latent tuberculosis infection (LTBI) may develop into active TB. Thus it is important to understand the mechanism of drug resistance, find new drugs, and find biomarkers for TB diagnosis. The rapid progress of metabolomics has enabled quantitative metabolite profiling of both the host and the pathogen. In this context, we provide recent progress in the application of metabolomics toward biomarker discovery for tuberculosis. In particular, we first focus on biomarkers based on blood or other body fluids for diagnosing active TB, identifying LTBI and predicting the risk of developing active TB, as well as monitoring the effectiveness of anti-TB drugs. Then we discuss the pathogen-based biomarker research for identifying drug resistant TB. While there have been many reports of potential candidate biomarkers, validations and clinical testing as well as improved bioinformatics analysis are needed to further substantiate and select key biomarkers before they can be made clinically applicable.

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Section: Pathogen-based Biomarkersmentioning

confidence: 99%

Biomarker discovery for tuberculosis using metabolomics

Jiang

2023

Front. Mol. Biosci.

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“…Mtp binds laminin [111] and has been implicated in the ability of M. tuberculosis to invade epithelial and macrophage cell lines in culture [179,180], but inactivation of mtp in two M. tuberculosis strains resulted in no change in the outcome of infection in C3HeB/FeJ mice that form necrotic, hypoxic lesions in which adherence to extracellular matrix proteins could play a role in mycobacterial colonization [175]. Nevertheless, recent studies have implicated Mtp deficiency in metabolic alterations in M. tuberculosis [181], macrophages [182], and epithelial cells [183]. Unlike Mtp, the mycobacterial Tad pilus has only been observed microscopically in one study and in its heterologously-expressed and purified crystalline form [174], but like for mtp inactivation, deletion of M. tuberculosis tad genes had no effect on virulence [175].…”

Section: Appendages and Lectinsmentioning

confidence: 99%

Mycobacterial Adhesion: From Hydrophobic to Receptor-Ligand Interactions

2022

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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.

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