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Pulmonary Tuberculosis II

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Fluorescence Assays for the Study of Mycobacterium tuberculosis Interaction with the Immune Receptor SLAMF1

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The Endogenous Retinoic Acid Receptor Pathway Is Exploited by Mycobacterium tuberculosis during Infection, Both

Yonne Karoline Tenório de Menezes¹, Carolina Eto¹, Joseana de Oliveira²

¹Laboratory of Immunobiology, Department of Microbiology, Immunology and Parasitology, Federal University of Santa Catarina, Florianópolis, Brazil.

Journal of Immunology (Baltimore, Md. : 1950)

|July 3, 2023

Summary

Mycobacterium tuberculosis infection activates the retinoic acid receptor (RAR) pathway, influencing immune cells. Inhibiting RARs reduced bacterial burden in mice, suggesting RARs as a therapeutic target for tuberculosis.

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Area of Science:

Immunology
Molecular Biology
Microbiology

Background:

Retinoic acid (RA) is a vitamin A metabolite crucial for immune regulation via nuclear RA receptors (RARs) and retinoid X receptors.
Mycobacterium tuberculosis (M.tb) infection models showed that live M.tb, but not heat-killed, robustly induces endogenous RAR pathway activation in THP-1 cells.
This suggests a specific interaction between M.tb and the host's RAR signaling pathway.

Purpose of the Study:

To investigate the role of endogenous RAR activity in M.tb infection.
To explore the potential of pharmacological RAR inhibition as an anti-tuberculosis strategy.

Main Methods:

In vitro studies using THP-1 cells and human primary CD14+ monocytes.
In vivo studies using a low-dose murine model of tuberculosis.
Pharmacological inhibition of RARs using a specific pan-RAR inverse agonist.

Main Results:

M.tb induces classical RA response element genes (e.g., CD38, DHRS3) in immune cells via a RAR-dependent pathway.
M.tb-stimulated RAR activation requires non-proteinaceous factors present in fetal bovine serum (FBS).
RAR blockade in mice significantly reduced specific alveolar macrophage populations and decreased lung mycobacterial burden twofold.

Conclusions:

The endogenous RAR activation axis is implicated in M.tb infection both in vitro and in vivo.
Targeting RAR signaling presents a potential novel therapeutic avenue for tuberculosis treatment.