CD206+macrophage is an accelerator of endometriotic-like lesion via promoting angiogenesis in the endometriosis mouse model

In endometriosis, M2 M Phi s are dominant in endometriotic lesions, but the actual role of M2 M Phi is unclear. CD206 positive (+) M Phi is classified in one of M2 type M Phi s and are known to produce cytokines and chemokines. In the present study, we used CD206 diphtheria toxin receptor mice, which enable to deplete CD206+ cells with diphtheria toxin (DT) in an endometriosis mouse model. The depletion of CD206+ M Phi decreased the total weight of endometriotic-like lesions significantly (p < 0.05). In the endometriotic-like lesions in the DT group, a lower proliferation of endometriotic cells and the decrease of angiogenesis were observed. In the lesions, the mRNA levels of VEGFA and TGF beta 1, angiogenic factors, in the DT group significantly decreased to approximately 50% and 30% of control, respectively. Immunohistochemical study revealed the expressions of VEGFA and an endothelial cell marker CD31 in lesions of the DT group, were dim compared to those in control. Also, the number of TGF beta 1 expressing M Phi was significantly reduced compared to control. These data suggest that CD206+ M Phi promotes the formation of endometriotic-like lesions by inducing angiogenesis around the lesions.

Automated summary

The study demonstrates that CD206+ MΦ promotes the formation of endometriotic-like lesions by inducing angiogenesis around the lesions. Depletion of CD206+ MΦ significantly reduces the total weight of lesions and angiogenesis.