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Macrophage Epithelial Reprogramming Underlies Mycobacterial Granuloma Formation and Promotes Infection.

Mark R Cronan¹, Rebecca W Beerman¹, Allison F Rosenberg¹

¹Department of Molecular Genetics and Microbiology, Duke University School of Medicine, Durham, NC 27710, USA.

|October 21, 2016

Summary

This summary is machine-generated.

Mycobacterium tuberculosis infection causes macrophages to adopt epithelial traits, forming granulomas. Disrupting this epithelial transition in macrophages improves host survival by altering infection dynamics.

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Isolation and In Vitro Culture of Murine and Human Alveolar Macrophages

Isolation and In Vitro Culture of Murine and Human Alveolar Macrophages

Published on: April 20, 2018

Area of Science:

Immunology
Cell Biology
Infectious Diseases

Background:

Tuberculosis (TB) is characterized by granulomas, organized immune cell aggregates.
Macrophage morphology changes within granulomas, but underlying molecular mechanisms are unknown.

Purpose of the Study:

To investigate the molecular and cellular programs driving macrophage reprogramming during mycobacterial granuloma formation.
To determine the role of epithelial reprogramming in granuloma structure and function.

Main Methods:

Utilized the zebrafish-Mycobacterium marinum infection model.
Analyzed macrophage-specific E-cadherin function disruption.
Examined granuloma structure, immune cell infiltration, bacterial burden, and host survival.

Main Results:

Mycobacterial infection induced epithelial molecules and structures in macrophages.
Macrophage reprogramming paralleled mesenchymal-epithelial transitions.
Disrupting E-cadherin in macrophages led to disordered granulomas, increased immune cell access, reduced bacterial load, and enhanced host survival.
Similar macrophage transformation was observed in human tuberculosis granulomas.

Conclusions:

Granuloma macrophages undergo significant reprogramming, adopting epithelial characteristics.
E-cadherin-mediated epithelial transition in macrophages plays a crucial role in granuloma formation and influences infection outcome.
The granuloma's structure, driven by macrophage epithelial reprogramming, can paradoxically protect bacteria, but disrupting this can benefit the host.