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Polarization of M1 and M2 Human Monocyte-Derived Cells and Analysis with Flow Cytometry upon Mycobacterium tuberculosis Infection
Published on: September 18, 2020
Mycobacterium tuberculosis induces CCL18 expression in human macrophages
G Ferrara1, B Bleck, L Richeldi
1Bellevue Chest Service, Division of Pulmonary and Critical Care Medicine, NYU School of Medicine, New York, NY, USA. giovanni.ferrara@unipg.it
Scandinavian Journal of Immunology
|October 31, 2008
Summary
Mycobacterium tuberculosis (MTB) infection significantly increases Chemokine (C-C motif) ligand 18 (CCL18) and Interleukin-10 (IL-10) in human macrophages. These molecules may recruit T cells and suppress immunity, potentially aiding early infection tolerance.
Area of Science:
- Immunology
- Microbiology
Background:
- Mycobacterium tuberculosis (MTB) interaction with the immune system involves cytokine and chemokine responses.
- Chemokine (C-C motif) ligand 18 (CCL18) and Interleukin-10 (IL-10) are key secreted factors.
- These factors are postulated to recruit naive T lymphocytes and inhibit pro-inflammatory responses.
Purpose of the Study:
- To investigate the role of CCL18 and IL-10 in an in vitro model of MTB infection in human macrophages.
Main Methods:
- Human CD14(+) monocytes were differentiated into monocyte-derived macrophages (MDM).
- MDM and alveolar macrophages were stimulated with lipopolysaccharide (LPS) and heat-killed MTB.
- CCL18 protein and mRNA levels were measured by ELISA and real-time PCR, IL-10 by ELISA.
Main Results:
- MTB stimulation significantly increased CCL18 protein and mRNA levels in MDM.
- Infected alveolar macrophages showed increased CCL18 production.
- IL-10 levels were significantly elevated in LPS- and MTB-stimulated cells.
Conclusions:
- Up-regulation of CCL18 and IL-10 in macrophages by MTB suggests involvement in naive T cell recruitment.
- This may contribute to local suppressive immunity against intracellular pathogens.
- This mechanism could facilitate immune tolerance during early MTB infection phases.
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