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MPEG1/perforin-2 mutations in human pulmonary nontuberculous mycobacterial infections

Ryan M McCormack1, Eva P Szymanski2, Amy P Hsu2

  • 1Department of Microbiology and Immunology, University of Miami School of Medicine, Miami, Florida, USA.

JCI Insight
|April 20, 2017
PubMed

Insights

Perforin-2, a key immune protein, is crucial for fighting bacterial infections. Genetic defects in perforin-2 (MPEG1) in humans can lead to increased susceptibility to persistent mycobacterial diseases.

Area of Science:

  • Immunology
  • Genetics
  • Microbiology

Background:

  • Perforin-2 is a conserved pore-forming protein essential for innate immunity.
  • Perforin-2-deficient mice exhibit susceptibility to bacterial infections.
  • No human diseases were previously linked to perforin-2 deficiencies.

Purpose of the Study:

  • To investigate the role of perforin-2 (MPEG1) in human susceptibility to intracellular bacterial infections.
  • To identify genetic variations in MPEG1 associated with persistent nontuberculous mycobacterial infections.

Main Methods:

  • Clinical evaluation of four patients with persistent nontuberculous mycobacterial infections.
  • Genetic analysis to identify heterozygous MPEG1 mutations.
  • In vitro functional assays of patient-derived immune cells (neutrophils, macrophages, B cells).
  • CRISPR mutagenesis to validate the impact of identified mutations.

Main Results:

  • Four patients with persistent nontuberculous mycobacterial infections carried heterozygous MPEG1 mutations.
  • Patient immune cells showed impaired killing of Mycobacterium avium in vitro.
  • CRISPR mutagenesis confirmed the detrimental effect of these mutations on antibacterial activity.
  • Perforin-2 haploinsufficiency was linked to reduced ability to control intracellular bacteria.

Conclusions:

  • Heterozygous mutations in MPEG1 (perforin-2) can cause human immunodeficiency.
  • Perforin-2 haploinsufficiency contributes to susceptibility to intracellular bacterial infections like nontuberculous mycobacteria.
  • This study identifies a novel genetic basis for susceptibility to mycobacterial diseases.

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