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.

Infection and Immunity
|December 30, 2016
PubMed

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.

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