ArticleThe Journal of biological chemistry2008
Identification of Mycobacterium tuberculosis clinical isolates with altered phagocytosis by human macrophages due to a truncated lipoarabinomannan.
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
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Who cites it
39 citing papers in PubMed, 67 citations in OpenAlex.
- Drug resistant Mycobacterium tuberculosis strains have altered cell envelope hydrophobicity that influences infection outcomes in human macrophages.Scientific reports · 2024Article
- Drug resistantbioRxiv : the preprint server for biology · 2024Article
- Pathogenicity and virulence ofVirulence · 2023Review
- Collected Thoughts on Mycobacterial Lipoarabinomannan, a Cell Envelope Lipoglycan.Pathogens (Basel, Switzerland) · 2023Review
- Drug-resistant strains ofFrontiers in cellular and infection microbiology · 2023Review
- Resistance and Susceptibility Immune Factors at Play duringPathogens (Basel, Switzerland) · 2022Review
- Tuberculosis Phenotypic and Genotypic Drug Susceptibility Testing and Immunodiagnostics: A Review.Frontiers in immunology · 2022Review
- Evolution of Drug-ResistantFrontiers in microbiology · 2021Review
- Comparative Structural Study of Terminal Ends of Lipoarabinomannan from Mice Infected Lung Tissues and Urine of a Tuberculosis Positive Patient.ACS infectious diseases · 2020Article
- Improved Alere Determine Lipoarabinomannan Antigen Detection Test for the Diagnosis of Human and Bovine Tuberculosis by Manipulating Urine and Milk.Scientific reports · 2019Article
- TheThe Biochemical journal · 2019Review
- Mycobacterial Evolution Intersects With Host Tolerance.Frontiers in immunology · 2019Review
- Underestimated Manipulative Roles ofFrontiers in immunology · 2019Review
- Mycobacterium tuberculosis carrying a rifampicin drug resistance mutation reprograms macrophage metabolism through cell wall lipid changes.Nature microbiology · 2018Article
- Updates on antibody functions in Mycobacterium tuberculosis infection and their relevance for developing a vaccine against tuberculosis.Current opinion in immunology · 2018Review
- PPARγ is critical for Mycobacterium tuberculosis induction of Mcl-1 and limitation of human macrophage apoptosis.PLoS pathogens · 2018Article
- Mannose-capped lipoarabinomannan in Mycobacterium tuberculosis pathogenesis.Pathogens and disease · 2018Review
- Mycobacterium tuberculosis universal stress protein Rv2623 interacts with the putative ATP binding cassette (ABC) transporter Rv1747 to regulate mycobacterial growth.PLoS pathogens · 2017Article
- Immunological consequences of strain variation within the Mycobacterium tuberculosis complex.European journal of immunology · 2017Review
- Article
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
Abstract
Phenotypically distinct clinical isolates of Mycobacterium tuberculosis are capable of altering the balance that exists between the pathogen and human host and ultimately the outcome of infection. This study has identified two M. tuberculosis strains (i.e. HN885 and HN1554) among a bank of clinical isolates with a striking defect in phagocytosis by primary human macrophages when compared with strain Erdman, a commonly used laboratory strain for studies of pathogenesis. Mass spectrometry in conjunction with NMR studies unequivocally confirmed that both HN885 and HN1554 contain truncated and more branched forms of mannose-capped lipoarabinomannan (ManLAM) with a marked reduction of their linear arabinan (corresponding mainly to the inner Araf-alpha(1-->5)-Araf unit) and mannan (with fewer 6-Manp residues and more substitutions in the linear Manp-alpha(1-->6)-Manp unit) domains. The truncation in the ManLAM molecules produced by strains HN885 and HN1554 led to a significant reduction in their surface availability. In addition, there was a marked reduction of higher order phosphatidyl-myo-inositol mannosides and the presence of dimycocerosates, triglycerides, and phenolic glycolipid in their cell envelope. Less exposed ManLAM and reduced higher order phosphatidyl-myo-inositol mannosides in strains HN885 and HN1554 resulted in their low association with the macrophage mannose receptor. Despite reduced phagocytosis, ingested bacilli replicated at a fast rate following serum opsonization. Our results provide evidence that the clinical spectrum of tuberculosis may be dictated not only by the host but also by the amounts and ratios of surface exposed mycobacterial adherence factors defined by strain genotype.
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Registered trials
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