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.