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Article

n-Butyl Benzyl Phthalate Exposure Promotes Lesion Survival in a Murine Endometriosis Model

by 1, 1, 1,2, 3,† and 1,4,5,*,†
1
Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 80708, Taiwan
2
Department of Obstetrics and Gynecology, Kaohsiung Medical University Hospital, Kaohsiung 80756, Taiwan
3
Department of Obstetrics and Gynecology, E-Da Hospital, I-Shou University, Kaohsiung 82445, Taiwan
4
Research Center for Environmental Medicine, Kaohsiung Medical University, Kaohsiung 80708, Taiwan
5
Department of Medical Research, Kaohsiung Medical University Hospital, Kaohsiung 80756, Taiwan
*
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Academic Editor: Jörg Lehmann
Int. J. Environ. Res. Public Health 2021, 18(7), 3640; https://doi.org/10.3390/ijerph18073640
Received: 3 March 2021 / Revised: 24 March 2021 / Accepted: 30 March 2021 / Published: 31 March 2021
(This article belongs to the Special Issue Current Insights into Immunotoxicology)
Endometriosis is an inflammatory and estrogen-dependent gynecological disease associated with exposure to environmental endocrine disruptors. n-Butyl benzyl phthalate (BBP), a ubiquitous plasticizer, has weak estrogenic activity, and exposure to BBP is associated with endometriosis. We aimed to elucidate the immunomodulatory effect of BBP on endometriosis development. We previously established a surgery-induced endometriosis-like murine model. In the present study, we exposed those mice to BBP 10 days prior to surgery and 4 weeks after surgery at physiologically relevant doses to mimic human exposure. Chronic exposure to BBP did not promote the growth of endometriotic lesions; however, the lesion survival rate in BBP-treated mice did increase significantly compared with control mice. Multiparametric flow cytometry showed that BBP exposure did not affect the homeostasis of infiltrated immune subsets in lesions but did enhance CD44 (adhesion marker) expression on plasmacytoid dendritic cells (pDCs). Blocking CD44 interactions locally inhibited endometriotic lesion growth. Immunofluorescence results further confirmed that CD44 blocking inhibited pDC infiltration and reduced the frequency of CD44+ pDCs in endometriotic tissues. BBP also disrupted the estrus cycle in these mice. This study suggests that chronic exposure to low-dose BBP may promote survival of endometriotic tissue through CD44-expressing pDCs. View Full-Text
Keywords: n-Butyl benzyl phthalate; CD44; dendritic cell; endometriosis n-Butyl benzyl phthalate; CD44; dendritic cell; endometriosis
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MDPI and ACS Style

Sharma, P.; Lee, J.-Y.L.; Tsai, E.-M.; Chang, Y.; Suen, J.-L. n-Butyl Benzyl Phthalate Exposure Promotes Lesion Survival in a Murine Endometriosis Model. Int. J. Environ. Res. Public Health 2021, 18, 3640. https://doi.org/10.3390/ijerph18073640

AMA Style

Sharma P, Lee J-YL, Tsai E-M, Chang Y, Suen J-L. n-Butyl Benzyl Phthalate Exposure Promotes Lesion Survival in a Murine Endometriosis Model. International Journal of Environmental Research and Public Health. 2021; 18(7):3640. https://doi.org/10.3390/ijerph18073640

Chicago/Turabian Style

Sharma, Pooja, Jo-Yu L. Lee, Eing-Mei Tsai, Yu Chang, and Jau-Ling Suen. 2021. "n-Butyl Benzyl Phthalate Exposure Promotes Lesion Survival in a Murine Endometriosis Model" International Journal of Environmental Research and Public Health 18, no. 7: 3640. https://doi.org/10.3390/ijerph18073640

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