A key cytokine in endometriosis can be targeted for endometriosis treatment

A French study shows macrophage migration inhibitory factor (MIF) can be a therapeutic target for endometriosis.

Key Points

Highlights:

• Studies showed that MIF has roles in the growth and progression of endometriosis lesions in mice, and treatment with MIF inhibitor, ISO-1, blocks the development of endometriosis pathology. These data suggest that MIF can be a promising therapeutic target for endometriosis. 

Importance:

• It is essential to identify new therapeutic targets for endometriosis as the current approaches are costly and more symptomatic than curative.
• Targeting MIF by its specific inhibitors may be a useful alternative to current treatment.

What’s done here?

• A review of data on the role of MIF in endometriosis.

Limitations of the study:

• This review reports the results from a limited number of studies conducted by the author’s laboratory. Further studies are needed to confirm the role of MIF in endometriosis and whether it can be an efficient target for endometriosis treatment.
• The primary study discussed here was done in mice, therefore, whether it applies to humans requires further investigation.

Lay Summary

Immune system dysfunction has been implicated in the development of endometriosis. One study showed that 95% of cells found in the peritoneal fluid of women with endometriosis are macrophages with impaired phagocytic function, which are unable to eat away unwanted cells, molecules, and other targets present in this fluid. This kind of failed immune surveillance is suspected to be involved in the growth and survival of endometrium outside of the uterus, which results in endometriosis. Macrophage migration inhibitory factor (MIF), a factor that blocks the migration of macrophages, are thought to be involved in this process.

MIF levels are found to be high in blood and peritoneal fluid of women with endometriosis. The levels correlated with the severity of the disease; i.e., higher levels were seen in more severe conditions. A previous study by the authors showed that treatment of mice with endometriosis with MIF inhibitor stopped the development of endometriosis further, and reduced the number of endometriotic lesions compared to the control animals. Likewise, when the mice genetically lacking MIF were compared to normal ones, the number and size of the endometriotic lesions were reduced significantly.

The data reviewed in this article suggests that MIF can be a valid therapeutic target for endometriosis – a more cost-efficient and potentially curative alternative to the current approaches according to the authors. The fact that MIF inhibitors exist and they are well tolerated by animals is promising for human studies to be conducted in the future.

Research Source: https://www.ncbi.nlm.nih.gov/pubmed/26481016