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Updated: May 12, 2026
Alveolar Macrophage Phagocytosis and Bacteria Clearance in Mice
Published on: March 2, 2019
The lpqS knockout mutant of Mycobacterium tuberculosis is attenuated in macrophages
Suba Sakthi1, Sujatha Narayanan
1Department of Immunology, National Institute for Research in Tuberculosis, Formerly Tuberculosis Research Centre, Chennai, India.
Abstract:
Lipoproteins of Mycobacterium tuberculosis (M. tuberculosis) represent an important class of cell envelop proteins. On the whole, 99 putative lipoproteins have been identified in the genome of M. tuberculosis. Earlier investigations on individual mycobacterial lipoproteins demonstrate that some lipoproteins elicit a strong immune response, while others are virulence factors in different models of infection. LpqS is an uncharacterized lipoprotein encoded by the open reading frame Rv0847 of M. tuberculosis. In the present study, we have characterized this putative lipoprotein LpqS with respect to the virulence of M. tuberculosis. A mutant of the M. tuberculosis H37Rv strain not producing LpqS (ΔlpqS) was generated by specialized transduction. The deletion mutant showed reduced growth in Sauton's minimal media and was highly sensitive to SDS and copper, compared to the wild type when grown on solid media. In vitro infection studies showed that the mutant was attenuated for growth in PMA-activated THP-1 cells. Complementation of the mutant with a single copy of the gene cloned under the hsp60 promoter partially restored the phenotype of the wild type strain H37Rv. Thus lpqS plays an important role in sensing the host macrophage environment and might be required for the intracellular survival of M. tuberculosis. Cotranscription of lpqS with the genes downstream cysK2, Rv0849 and Rv0850 was also demonstrated by Reverse transcription PCR (RT-PCR) of intergenic regions.
Insights
Mycobacterium tuberculosis lipoprotein LpqS is crucial for bacterial growth and survival within host macrophages. Deleting lpqS impairs M. tuberculosis virulence, highlighting its role in sensing the host environment.
Area of Science:
- Microbiology
- Molecular Biology
- Immunology
Background:
- Lipoproteins are key cell envelope components in Mycobacterium tuberculosis.
- Some lipoproteins act as virulence factors or elicit immune responses.
- LpqS (Rv0847) is a previously uncharacterized lipoprotein in M. tuberculosis.
Purpose of the Study:
- To characterize the role of the M. tuberculosis lipoprotein LpqS in bacterial virulence.
- To investigate the function of LpqS in the context of host-pathogen interactions.
Main Methods:
- Generation of an M. tuberculosis H37Rv deletion mutant lacking LpqS (ΔlpqS) using specialized transduction.
- Phenotypic characterization of the ΔlpqS mutant, including growth assays (Sauton's media, solid media with SDS/copper) and in vitro infection studies (PMA-activated THP-1 cells).
- Complementation studies and Reverse transcription PCR (RT-PCR) to confirm cotranscription.
Main Results:
- The ΔlpqS mutant exhibited reduced growth in minimal media and increased sensitivity to SDS and copper on solid media.
- In vitro infection assays demonstrated attenuated growth of the ΔlpqS mutant in THP-1 macrophages.
- Complementation partially restored the wild-type phenotype, and cotranscription of lpqS with downstream genes was confirmed.
Conclusions:
- LpqS plays a significant role in the virulence of Mycobacterium tuberculosis.
- LpqS is important for sensing the host macrophage environment and intracellular survival.
- The findings provide insights into the function of lipoproteins in M. tuberculosis pathogenesis.
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