Receptor Biology and Signal Transduction

ORF19-05 - The Role of Exposure to Environmental Toxicants and Their Effect on Immune Cells in the Development of Endometriosis

Saturday, June 13, 2026

4:00 PM - 4:15 PM CT

Location: Room W180

Oral Abstract Presenter(s)

Lateia Taylor, MD (she/her/hers)

UNIVERSITY OF CINCINNATI - MSB R005B
West Chester, OH, United States

Senior Author/Primary Investigator(s)

KB

Katherine Burns, PhD

University of Cincinnati
Cincinnati, Ohio, United States

Co-Author(s)

SM

Stephanie Morris, BS

Research Assoicate
University of Cincinnati
Cincinnati, Ohio, United States
TW

Taylor Wilson, MS

University of Cincinnati
Cincinnati, United States
MT

Michael Thomas, MD

University of Cincinnati
Cincinnati, Ohio, United States

Disclosure(s):

Lateia Taylor, MD: No financial relationships to disclose

Background: While the etiology of endometriosis (EMS) remains unknown, a prevailing hypothesis is that disease occurs via retrograde menstruation. Correlative studies suggest environmental toxicant exposures contribute to disease development and/or progression. Per- and – poly-fluorinated alkylated substances (PFASs) are implicated in EMS, as they are present in many water-resistant products including menstrual products. In particular, two legacy PFASs, perfluoroactane sulfonic acid (PFOS) and perfluorooctanoic acid (PFOA), are implicated in EMS. Findings from our mouse model of EMS demonstrate PFOA is an immunotoxicant that may promote EMS via macrophage-mediated peroxisome proliferator activated receptor (PPAR) signaling.

Objective: The aim of this project is to evaluate immune cell participation in PFOA- and PFOS-mediated EMS development and to determine the crosstalk between PFAS and PPAR signaling that alters gene expression in EMS lesion development using a mouse model.
MATERIALS AND

Methods: Our mouse model of EMS was used to examine the systemic affect of PFASs on macrophage trafficking and EMS lesions. Mice were treated with PFOA (n= 4) or PFOS (n= 6) by gavage for up to 6 weeks. Mice were euthanized in estrus. The peritoneal fluid was collected for differentials and stained with modified Geimsa. Immune cell evaluation was performed using basic microscopy. Lesion sections were stained to examine macrophage recruitment with F4/80 by immunohistochemistry. To examine the crosstalk between PFAS and PPAR in lesions, lesion RNA will be analyzed for: Ppara, Ppar target genes, macrophages, macrophage associate cytokines, and genes known to be involved in EMS. One way ANOVA (p < 0.05).

Results: A difference in the number of activated peritoneal macrophages in both PFOA and PFOS treated groups was found with a greater increase in the PFOA-treated group compared to control. Similarly, in the lesions, the PFOA-treated group compared to control-treated had increased macrophage recruitment. Together, these findings suggest an increase in macrophage recruitment which indicates an inflammatory response. We anticipate PPAR target gene expression to be upregulated in PFOA-treated mice compared to control-treated, confirming an immunotoxicant role in the development of EMS lesions.

Conclusions: Our data provides evidence that PFASs, PFOA in particular more so than PFOS, contributes to and/or exasperates a chronic inflammatory environment that occurs via macrophage-mediated PPAR signaling. Together, these downstream immunotoxiacnt effects likely contribute to the onset of EMS and progression of disease. Limiting exposure to PFASs may help decrease chronic inflammation that contributes to EMS.

*Unless otherwise noted, all abstracts presented at ENDO must not be released to the press or the public until the date and time of presentation. For oral presentations, the abstracts are embargoed until the session begins. The Endocrine Society reserves the right to lift the embargo on specific abstracts that are selected for promotion prior to or during ENDO.*