Related Experiment Video
Updated: Aug 28, 2026

Bone Marrow-derived Macrophage Production
Published on: November 22, 2013
Mycobacterium bovis Requires P27 (LprG) To Arrest Phagosome Maturation and Replicate within Bovine Macrophages
Cristina Lourdes Vázquez1, María Verónica Bianco1, Federico Carlos Blanco1
1Instituto de Biotecnología, CICVyA-INTA, Nicolás Repetto y De Los Reseros, Buenos Aires, Argentina.
Abstract:
Mycobacterium bovis causes tuberculosis in a wide variety of mammals, with strong tropism for cattle and eventually humans. P27, also called LprG, is among the proteins involved in the mechanisms of the virulence and persistence of M. bovis and Mycobacterium tuberculosis Here, we describe a novel function of P27 in the interaction of M. bovis with its natural host cell, the bovine macrophage. We found that a deletion in the p27-p55 operon impairs the replication of M. bovis in bovine macrophages. Importantly, we show for the first time that M. bovis arrests phagosome maturation in a process that depends on P27. This effect is P27 specific since complementation with wild-type p27 but not p55 fully restored the wild-type phenotype of the mutant strain; this indicates that P55 plays no important role during the early events of M. bovis infection. In addition, we also showed that the presence of P27 from M. smegmatis decreases the association of LAMP-3 with bead phagosomes, indicating that P27 itself blocks phagosome-lysosome fusion by modulating the traffic machinery in the cell host.
Insights
Mycobacterium bovis uses the P27 protein to block phagosome maturation in bovine macrophages, a key step for its survival and persistence. This finding reveals a novel virulence mechanism for M. bovis.
Area of Science:
- Microbiology
- Immunology
- Cell Biology
Background:
- Mycobacterium bovis causes tuberculosis in mammals, including cattle and humans.
- The P27 protein (LprG) is implicated in the virulence and persistence of M. bovis and M. tuberculosis.
Purpose of the Study:
- To investigate the novel function of P27 in the interaction between M. bovis and bovine macrophages.
- To elucidate the role of P27 in the early stages of M. bovis infection.
Main Methods:
- Genetic manipulation of M. bovis to create a deletion in the p27-p55 operon.
- Infection of bovine macrophages with wild-type and mutant M. bovis strains.
- Analysis of phagosome maturation and phagosome-lysosome fusion.
Main Results:
- A deletion in the p27-p55 operon impaired M. bovis replication in bovine macrophages.
- M. bovis arrests phagosome maturation in a P27-dependent manner.
- P27, but not P55, was responsible for blocking phagosome maturation, indicating P55's limited role in early infection events.
- P27 modulates host cell machinery to inhibit phagosome-lysosome fusion.
Conclusions:
- P27 is crucial for M. bovis to evade host immune responses by preventing phagosome maturation.
- P27's ability to block phagosome-lysosome fusion is a key virulence factor for M. bovis persistence in bovine macrophages.
- Targeting P27 could be a potential strategy to combat M. bovis infections.
More Related Videos
08:34Identification of Virulence Markers of Mycobacterium abscessus for Intracellular Replication in Phagocytes
Published on: September 27, 2018
06:26Author Spotlight: Optimizing CFU Determination for Efficient Assessment of TB Vaccine Efficacy and Antigen Presentation Analysis
Published on: July 28, 2023
Related Concept Videos
Lysogenic Cycle of Bacteriophages
Pulmonary Tuberculosis II
Here is a detailed explanation of its pathophysiology:
Transmission: The process begins when a person inhales droplet nuclei containing M. tuberculosis. These are typically released into the air when an individual with pulmonary or...
Regulation of Bacterial Virulence
Tuberculosis