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Updated: Jun 3, 2025
Macrophage Differentiation and Polarization into an M2-Like Phenotype using a Human Monocyte-Like THP-1 Leukemia Cell Line
Published on: August 2, 2021
Parvimonas micra-polarized M2-like tumor-associated macrophages accelerate colorectal cancer development via IL-8
Dang Khoa Nguyen1,2,3, Min-Jung Kang1, Su-Jeong Oh1,2,3
1Department of Oral Biochemistry, Dental and Life Science Institute, School of Dentistry, Pusan National University, Yangsan, Republic of Korea.
Abstract:
Parvimonas micra (Pm), a periodontal pathogen, has been implicated in the impairment of anti-tumor responses in colorectal cancer (CRC). The tumor microenvironment in CRC involves tumor-associated macrophages (TAMs), which are pivotal in modulating tumor-associated immune responses. The polarization of TAMs towards an M2-like phenotype promotes CRC progression by suppressing the immune system. However, the mechanisms by which Pm affects the progression of CRC remain inadequately elucidated. In this study, we explored the impact of Pm infection on CRC cell characteristics, including proliferation, chemoresistance, migration, and macrophage polarization. We found that Pm-infected THP-1-derived macrophages exhibited elevated interleukin-10 levels, a well-established M2 marker. Conditioned media from Pm-treated THP-1 cells significantly enhanced CRC cell proliferation, cisplatin resistance, and migration, and interleukin-8 was identified as a key factor. Consistent with the in vitro results, an azoxymethane/dextran sodium sulfate mouse model treated with oral Pm showed accelerated CRC tumor growth. These results offer mechanistic insights into the influence of Pm infection on tumor microenvironment in CRC through M2-like macrophage polarization. The identified pathways may serve as potential targets for therapeutic interventions for CRC.
Insights
Parvimonas micra (Pm) infection promotes colorectal cancer (CRC) progression by polarizing macrophages to an M2-like state, enhancing tumor cell proliferation and migration. This study reveals mechanisms linking Pm to CRC advancement via the tumor microenvironment.
Area of Science:
- Microbiology
- Immunology
- Oncology
Background:
- Parvimonas micra (Pm) is a periodontal pathogen linked to impaired anti-tumor immunity in colorectal cancer (CRC).
- Tumor-associated macrophages (TAMs) influence CRC progression, with M2-like polarization suppressing anti-tumor immune responses.
- Mechanisms of Pm's impact on CRC progression are not fully understood.
Purpose of the Study:
- To investigate the effects of Pm infection on CRC cell characteristics and macrophage polarization.
- To elucidate the role of Pm in modulating the CRC tumor microenvironment.
Main Methods:
- In vitro studies using THP-1 derived macrophages and CRC cells treated with Pm.
- Analysis of macrophage polarization markers (e.g., interleukin-10).
- In vivo studies using an azoxymethane/dextran sodium sulfate mouse model of CRC treated with oral Pm.
Main Results:
- Pm-infected macrophages showed increased interleukin-10 (M2 marker).
- Conditioned media from Pm-treated cells enhanced CRC cell proliferation, cisplatin resistance, and migration, with interleukin-8 identified as a key mediator.
- Oral Pm administration accelerated CRC tumor growth in a mouse model.
Conclusions:
- Pm infection promotes CRC progression by inducing M2-like macrophage polarization.
- Pm influences CRC cell proliferation, chemoresistance, and migration through factors like interleukin-8.
- These findings offer insights into Pm's role in the CRC tumor microenvironment and suggest potential therapeutic targets.
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