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Micah D Dunlap1, Shabaana A Khader1

  • 1Departments of Molecular Microbiology, Pathology, and Immunology, Washington University in St. Louis School of Medicine, Saint Louis, MO 63110, USA.

Cell Host & Microbe
|September 15, 2017
PubMed

Insights

Mycobacterium leprae infection causes nerve demyelination by triggering mitochondrial damage. Infected macrophages patrol nerve axons, leading to nerve cell demyelination and contributing to leprosy pathogenesis.

Area of Science:

  • Neuroscience
  • Immunology
  • Microbiology

Background:

  • Leprosy pathogenesis involves Mycobacterium leprae infection.
  • The mechanism of demyelination in leprosy has been unclear.

Purpose of the Study:

  • To elucidate how Mycobacterium leprae infection causes demyelination.
  • To investigate the role of macrophages in leprosy-induced nerve damage.

Main Methods:

  • Utilized a zebrafish model for Mycobacterium leprae infection.
  • Observed the interaction between infected macrophages and nerve axons.

Main Results:

  • Infected macrophages were found to patrol nerve axons.
  • This patrolling behavior triggered mitochondrial damage in nerve cells.
  • Induced demyelination of nerve cells was observed.

Conclusions:

  • Macrophages play a key role in Mycobacterium leprae-induced demyelination.
  • Mitochondrial damage is a critical step in leprosy-related nerve pathology.

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