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Proliferation and Differentiation of Murine Myeloid Precursor 32D/G-CSF-R Cells
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CSF1/CSF1R signaling mediates malignant pleural effusion formation
Chrysavgi N Kosti1, Photene C Vaitsi1, Apostolos G Pappas1
1Marianthi Simou Laboratory, 1st Department of Critical Care and Pulmonary Medicine, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece.
JCI Insight
|March 22, 2022
Summary
Targeting CSF1R+ M2 macrophages and CSF1R signaling can limit malignant pleural effusion (MPE). Inhibiting CSF1R reduces vascular permeability and tumor progression, offering a new therapeutic strategy for MPE.
Area of Science:
- Oncology
- Immunology
- Vascular Biology
Background:
- Malignant pleural effusion (MPE) is a common, incurable complication of many cancers.
- Tumor-associated macrophages, particularly M2 macrophages, are key players in MPE formation and are linked to poor prognosis.
- CSF1/CSF1 receptor (CSF1R) signaling drives M2 macrophage polarization.
Purpose of the Study:
- To investigate the role of CSF1R+ M2 macrophages in MPE development.
- To evaluate the therapeutic potential of targeting CSF1R signaling in experimental MPE models.
Main Methods:
- Generated mice with CSF1R-deficient macrophages.
- Induced lung and colon adenocarcinoma-associated MPE in mice.
- Administered a CSF1R inhibitor (BLZ945) to experimental MPE models.
Main Results:
- CSF1R+ macrophages enhance MPE by increasing vascular permeability, destabilizing tumor vessels, and promoting immune suppression.
- CSF1R inhibition reduced MPE, vascular permeability, and neoangiogenesis, while impeding tumor progression.
- CSF1R signaling in cancer-associated fibroblasts contributes to MPE by influencing macrophage properties.
Conclusions:
- CSF1R+ M2 macrophages are critical drivers of MPE.
- Targeting the CSF1/CSF1R axis is a promising therapeutic strategy for managing MPE.
- Inhibition of CSF1R impacts both macrophage and cancer-associated fibroblast functions to limit MPE.
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