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Polarization of M1 and M2 Human Monocyte-Derived Cells and Analysis with Flow Cytometry upon Mycobacterium tuberculosis Infection
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Monocytic myeloid-derived suppressor cells reflect tuberculosis severity and are influenced by cyclooxygenase-2

Marthe Jøntvedt Jørgensen1,2, Synne Jenum2, Kristian Tonby1,2

  • 1Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway.

Journal of Leukocyte Biology
|November 6, 2020
PubMed

Insights

Cyclooxygenase-2 inhibitors (COX-2i) showed limited in vivo effects on myeloid-derived suppressor cells (MDSCs) in tuberculosis patients. However, in vitro studies revealed that COX-2i reduced M-MDSC cytokine production.

Area of Science:

  • Immunology
  • Infectious Diseases
  • Pharmacology

Background:

  • Myeloid-derived suppressor cells (MDSCs) are elevated in tuberculosis (TB) and represent a potential target for host-directed therapy (HDT).
  • Understanding the impact of therapeutic agents on MDSCs is crucial for developing effective TB treatments.

Purpose of the Study:

  • To investigate the effects of cyclooxygenase-2 inhibitors (COX-2i) on monocytic MDSCs (M-MDSCs) in patients with TB.
  • To evaluate the in vitro impact of COX-2i on M-MDSCs and their interaction with Mycobacterium bovis.

Main Methods:

  • Flow cytometry was used to analyze M-MDSC frequencies and marker expression in blood from TB patients undergoing COX-2i treatment.
  • An in vitro model of mycobacterial infection was employed to assess COX-2i effects on M-MDSCs and bacterial uptake.

Main Results:

  • M-MDSC frequencies correlated with TB disease severity.
  • In vivo, COX-2i treatment led to reduced M-MDSC and IDO expression.
  • In vitro, M-MDSCs internalized Mycobacterium bovis, and infection increased COX-2, PD-L1, and Arginase-1 expression. COX-2i reduced M-MDSC cytokine production (IL-1β, IL-10, S100A9).

Conclusions:

  • COX-2i demonstrated limited in vivo efficacy on M-MDSCs in TB patients but reduced their cytokine production in vitro.
  • Further research is needed to explore the potential of COX-2i as part of a host-directed therapy strategy for TB.
Keywords:
M-MDSCMycobacteriacyclooxygenase-2 inhibitorhost directed therapyinnate immunity

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