Thymic stromal lymphopoietin contributes to endometriotic lesion proliferation and disease-associated inflammation.

Stanimira Aleksieva, Harshavardhan Lingegowda, Danielle J Sisnett, Alison McCallion, Katherine B Zutautas, Timothy Childs, Bruce A. Lessey, Chandrakant Tayade
In: bioRxiv · 2024 · doi:10.1101/2024.04.18.590132 · W4395013133
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This study found elevated thymic stromal lymphopoietin in endometriotic lesions, which promotes lesion proliferation and Th2 inflammation by reducing apoptosis and increasing proliferation in cell lines and mouse models.

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Abstract

Endometriosis is a chronic disorder in which endometrial-like tissue presents outside the uterus. Patients with endometriosis have been shown to exhibit aberrant immune responses within the lesion microenvironment and in circulation which contribute to the development of endometriosis. Thymic stromal lymphopoietin (TSLP) is an alarmin involved in cell proliferation and the induction of Th2 inflammation in various diseases, such as asthma, atopic dermatitis, pancreatic and breast cancer. Recent studies have detected TSLP within endometriotic lesions and shown that its concentrations are elevated in the peritoneal fluid of patients compared to controls. However, its role in disease pathophysiology remains unclear. Here, we compared TSLP expression in endometriotic lesions to matched patient endometrium and control endometrium samples. We also assessed its effect on the proliferation and apoptosis of human endometriosis-representative cell lines, as well as on lesion development and inflammation in a mouse model of the disease. We demonstrated that TSLP expression was elevated in the stroma of patient endometriotic lesions compared to control endometrial samples. In cell lines, TSLP treatment reduced the apoptosis of endometrial stromal cells and promoted the proliferation of THP-I cells. In mice induced with endometriosis, TSLP treatment induced a Th2 immune response within the lesion microenvironment, and led to TSLP receptor modulation in macrophages, dendritic cells, and CD4+ T cells. Furthermore, treatment increased murine endometriotic lesion proliferation. Overall, these results suggest that TSLP modulates the endometriotic lesion microenvironment and promotes a Th2 immune response that could support lesion development.

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endometriosis

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