A potential role for colony-stimulating factor 1 in the genesis of the early endometriotic lesion

To investigate the role(s) of colony-stimulating factor 1 (CSF-1) on the development of early endometriosis in a murine model by comparing rate of lesion formation in mice [1] homozygous for a CSF-1 mutation versus syngeneic controls and [2] after treatment with imatinib, a commercially available tyrosine kinase inhibitor that alters interaction(s) between CSF-1 and its receptor, c-fms.

Prospective, placebo-controlled animal study.

Academic medical center.

Six- to 8-week old female FVB, wild-type C57BL/6, and CSF-1 op/op mice.

Endometrial tissue from donor mice was used to induce endometriosis in murine recipients. In some experiments, mice homozygous for a CSF-1 mutation (CSF-1 op/op) were donors or recipients. In other experiments, donor and/or recipient mice received imatinib.

Histologic confirmation of endometriosis, rate of lesion formation.

By 40 hours, recipient mice developed a mean of 7.2 +/- 0.9 endometriotic lesions that had invaded host surfaces, and mesothelial cells had proliferated over the entire surface of the implants. The CSF-1 op/op mice developed significantly fewer (mean 0.9 +/- 0.3) endometriotic lesions versus syngeneic controls. Imatinib treatment resulted in significantly fewer lesions when compared with sham-treated controls.

Colony-stimulating factor 1 has a role in establishing early endometriotic lesions. Agents targeting CSF-1 or its actions have therapeutic potential for treating endometriosis.