ArticleMicrobes and infection2006
Comparative investigation of the pathogenicity of three Mycobacterium tuberculosis mutants defective in the synthesis of p-hydroxybenzoic acid derivatives.
Article in Microbes and infection, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 26 citations in OpenAlex.
- Bioorthogonal Metabolic Labeling of the Virulence Factor Phenolic Glycolipid in Mycobacteria.ACS chemical biology · 2024Article
- Sub-Lineage Specific Phenolic Glycolipid Patterns in theFrontiers in microbiology · 2022Article
- Poor stimulation of bovine dendritic cells byInnate immunity · 2020Article
- Playing hide-and-seek with host macrophages through the use of mycobacterial cell envelope phthiocerol dimycocerosates and phenolic glycolipids.Frontiers in cellular and infection microbiology · 2014Article
- Virulence and immune response induced by Mycobacterium avium complex strains in a model of progressive pulmonary tuberculosis and subcutaneous infection in BALB/c mice.Infection and immunity · 2013Article
- Article
- Modulation of cell death by M. tuberculosis as a strategy for pathogen survival.Clinical & developmental immunology · 2011Article
- Identification of a novel multidrug efflux pump of Mycobacterium tuberculosis.Antimicrobial agents and chemotherapy · 2008Article
Corrections and comments
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Authors and funding
23 authors at 4 institutions in 3 countries.
Funding
Abstract
p-Hydroxybenzoic acid derivatives (p-HBADs) are glycoconjugates secreted by all Mycobacterium tuberculosis isolates whose contribution to pathogenicity remains to be determined. The pathogenicity of three transposon mutants of M. tuberculosis deficient in the biosynthesis of some or all forms of p-HBADs was studied. Whilst the mutants grew similarly to the wild-type strain in macrophages and C57BL/6 mice, two of the mutants induced a more severe and diffuse inflammation in the lungs. The lack of production of some or all forms of p-HBADs in these two mutants also correlated with an increased secretion of the pro-inflammatory cytokines tumour-necrosis factor alpha, interleukin 6 and interleukin 12 in vivo. We propose that the loss of production of p-HBADs by tubercle bacilli results in their diminished ability to suppress the pro-inflammatory response to infection and that this ultimately provokes extensive pulmonary lesions in the C57BL/6 model of tuberculosis infection.
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