Related Experiment Video
Updated: Aug 3, 2026
Macrophage Cholesterol Depletion and Its Effect on the Phagocytosis of Cryptococcus neoformans
Published on: December 19, 2014
PPARγ Ameliorates Mycobacterium tuberculosis H37Ra-Induced Foamy Macrophage Formation via the ABCG1-Dependent
Yutao Ye1, Jun Liu1, Yang Guo1
1Jiangxi Province Key Laboratory of Laboratory Medicine, Department of Clinical Laboratory, The First Affiliated Hospital of Nanchang University, Nanchang, China.
Abstract:
Foamy macrophages are present during the course of Mycobacterium tuberculosis (Mtb) infection and seems to be nutrient-rich reservoir and secure reservoir for the bacilli, which leads to bacterial persistence and infection transmission. Peroxisome proliferator activated receptor γ (PPARγ) is a key transcription factor for cholesterol metabolism in macrophages and its role in regulating atherosclerosis related foamy macrophages (FMs) formation has been well-studied. However, knowledge about the mechanism of PPARγ regulating Mtb infection induced FM formation remains very limited. In this study, we investigate the functional role of PPARγ in Mtb H37Ra infection-induced foamy macrophages formation. H37Ra infection induced a time-dependent decreased expression of PPARγ that paralleled the augmented lipid body formation in THP1-derived macrophages. PPARγ antagonist GW9662 significantly potentiate H37Ra induced lipid body formation and inhibit ABCG1 expression, overexpression of ABCG1 by transduced macrophages with lentivirus significantly reversed the promotion effect of GW9662 on FM formation. Moreover, Treatment with a TLR2 neutralizing antibody ameliorated the activation of ABCG1 by Mtb H37Ra without significantly effecting the suppression of PPARγ, suggesting a greater role for TLR2 to regulate ABCG1 compared to PPARγ. Overall, this study showed that PPARγ is involved in ameliorating FM formation by regulating ABCG1 expression, these observations expose a novel role of PPARγ in the Mtb infection induced FM formation.
Insights
Peroxisome proliferator activated receptor γ (PPARγ) helps reduce foamy macrophage formation during Mycobacterium tuberculosis infection by regulating ABCG1 expression. This reveals a new role for PPARγ in combating tuberculosis persistence.
Area of Science:
- Immunology
- Cell Biology
- Microbiology
Background:
- Foamy macrophages harbor Mycobacterium tuberculosis (Mtb), promoting bacterial persistence and transmission.
- Peroxisome proliferator activated receptor γ (PPARγ) regulates cholesterol metabolism and foamy macrophage formation in atherosclerosis.
- The role of PPARγ in Mtb-induced foamy macrophage formation is not well understood.
Purpose of the Study:
- To investigate the functional role of PPARγ in Mycobacterium tuberculosis H37Ra infection-induced foamy macrophage formation.
Main Methods:
- THP1-derived macrophages were infected with Mtb H37Ra.
- PPARγ expression and lipid body formation were assessed over time.
- PPARγ antagonist GW9662 and ABCG1 overexpression were used to study regulatory mechanisms.
- TLR2 neutralizing antibody was employed to investigate TLR2's role.
Main Results:
- Mtb H37Ra infection decreased PPARγ expression and increased lipid body formation in a time-dependent manner.
- GW9662 potentiated Mtb-induced foamy macrophage formation and inhibited ABCG1 expression.
- ABCG1 overexpression reversed the pro-foamy macrophage effects of GW9662.
- TLR2 activation by Mtb influenced ABCG1 but not PPARγ suppression.
Conclusions:
- PPARγ ameliorates foamy macrophage formation during Mtb infection by regulating ABCG1 expression.
- This study identifies a novel role for PPARγ in Mtb infection-induced foamy macrophage formation.
More Related Videos
10:43Polarization of M1 and M2 Human Monocyte-Derived Cells and Analysis with Flow Cytometry upon Mycobacterium tuberculosis Infection
Published on: September 18, 2020
07:42Fluorescence Assays for the Study of Mycobacterium tuberculosis Interaction with the Immune Receptor SLAMF1
Published on: February 28, 2025
