Polarization of M2 Macrophages by Interaction between Prostate Cancer Cells Treated with Trichomonas vaginalis and Adipocytes.
M2 polarization
Trichomonas vaginalis
adipocyte
macrophage
prostate cancer
Journal
The Korean journal of parasitology
ISSN: 1738-0006
Titre abrégé: Korean J Parasitol
Pays: Korea (South)
ID NLM: 9435800
Informations de publication
Date de publication:
Jun 2020
Jun 2020
Historique:
received:
19
12
2019
accepted:
12
05
2020
entrez:
4
7
2020
pubmed:
4
7
2020
medline:
4
9
2020
Statut:
ppublish
Résumé
Trichomonas vaginalis causes inflammation of the prostate and has been detected in tissues of prostate cancers (PCa), prostatitis and benign prostatic hyperplasia. Obesity is a risk factor for PCa and causes a chronic subclinical inflammation. This chronic inflammation further exacerbates adipose tissue inflammation as results of migration and activation of macrophages. Macrophages are the most abundant immune cells in the PCa microenvironment. M2 macrophages, known as Tumor-Associated Macrophages, are involved in increasing cancer malignancy. In this study, conditioned medium (TCM) of PCa cells infected with live trichomonads contained chemokines that stimulated migration of the mouse preadipocytes (3T3-L1 cells). Conditioned medium of adipocytes incubated with TCM (ATCM) contained Th2 cytokines (IL-4, IL-13). Macrophage migration was stimulated by ATCM. In macrophages treated with ATCM, expression of M2 markers increased, while M1 markers decreased. Therefore, it is suggested that ATCM induces polarization of M0 to M2 macrophages. In addition, conditioned medium from the macrophages incubated with ATCM stimulates the proliferation and invasiveness of PCa. Our findings suggest that interaction between inflamed PCa treated with T. vaginalis and adipocytes causes M2 macrophage polarization, so contributing to the progression of PCa.
Identifiants
pubmed: 32615735
pii: kjp.2020.58.3.217
doi: 10.3347/kjp.2020.58.3.217
pmc: PMC7338904
doi:
Substances chimiques
Chemokines
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
217-227Subventions
Organisme : National Research Foundation of Korea
ID : 2017R1A2B4002072
Organisme : Ministry of Science and ICT
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