The Elimination of a Certain Type of Bacteria Suggests a New Endometriosis Treatment

A research group from the Graduate School of Medicine and iGCORE at Nagoya University in Japan has found that using an antibiotic against Fusobacterium reduces the formation of lesions associated with endometriosis, a gynecological condition in which endometrial tissue, which is normally found in the uterus, begins to grow outside of it. Their results suggest an alternative treatment for this condition. The study was published in Science Translational Medicine.

Targeting Fusobacterium Could be an Effective Non-Hormonal Antibiotic Treatment for Endometriosis

Endometriosis affects one in ten women aged between 15 and 49 years. The condition can cause lifelong health problems, including pelvic pain and infertility. Although endometriosis can be treated using hormone therapies and surgical resection, these methods sometimes lead to side effects, relapses and a significant impairment of pregnancy.

The group led by Professor Yutaka Kondo and Assistant Professor Ayako Muraoka of the Nagoya University Graduate School of Medicine, in collaboration with the National Cancer Center, found that the uterus of mice infected with Fusobacterium had more and more severe lesions. However, mice that had been given an antibiotic to eradicate Fusobacterium were observed to have improved lesion formation. The team’s findings strongly suggest that targeting Fusobacterium could be an effective non-hormonal antibiotic treatment for endometriosis.

The Role of Protein Transgelin (TAGLN)

Eradication of this bacterium through antibiotic treatment could be an approach to treating endometriosis in women who test positive for Fusobacterium infection, and such women could be readily identified by a vaginal swab or uterine smear. This study also highlights the usefulness of looking at upstream events to identify the causative pathogen.

The first finding was that a protein called Transgelin (TAGLN) was often upregulated in patients with endometriosis. This was not surprising, as the protein is associated with processes important for the development of endometriosis. However, this finding led to the conclusion that transforming growth factor beta (TGF-β) appeared to cause the upregulation of TAGLN.

Since TGF-β is released by macrophages, the body’s natural inflammatory inhibitors and immune regulatory cells, they concluded that these macrophages were activated in response to Fusobacterium. These data provide a strong and novel rationale for considering Fusobacterium as a non-hormonal, antibiotic-based treatment for endometriosis.