A prominent environmental endocrine disruptor, 4-nonylphenol, promotes endometriosis development via plasmacytoid dendritic cells

Pooja Sharma, Hsin-Han Tseng, Jo-Yu Lynn Lee, Eing-Mei Tsai, Eing‐Mei Tsai, Jau-Ling Suen, Jau‐Ling Suen
Molecular human reproduction · 2020 · vol. 26(8) , pp. 601–614 · doi:10.1093/molehr/gaaa039 · PMID:32497202 · W3033141987
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4-nonylphenol exposure promoted endometriotic lesion growth and pDC accumulation by enhancing IL-10 secretion from CD36-expressing pDCs.

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Abstract

Endometriosis is an estrogen-dependent chronic inflammatory disease and is associated etiologically with environmental endocrine disruptor (EED) exposure. 4-nonylphenol (NP), a widely found EED, has weak estrogenic activity and modulates plasmacytoid dendritic cell (pDC) function in vitro and in vivo. We aimed to elucidate the immunomodulatory effect of NP on the development of endometriosis, particularly focusing on pDCs. This study established a surgically induced endometriosis murine model (C57BL/6) under conditions of NP treatment that are relevant to the level and route of human exposure. Multi-parametric flow cytometry was used for analysis of infiltrated immune cell subsets in lesions. The results showed that NP exposure significantly promoted endometriotic lesion growth, survival and angiogenesis development of lesions as well as pDC accumulation in the lesions in mice. Adoptive transfer of NP-conditioned pDCs into mice significantly enhanced lesion development and local pDC infiltration, whereas NP-conditioned conventional dendritic cells did not affect lesion growth. In vitro functional analysis showed that NP-conditioned pDCs in lesions expressed high levels of CD36, a scavenger receptor and NP-conditioned splenic pDCs secreted an enhanced level of IL-10 in response to apoptotic cell recognition in a CD36-dependent manner. Furthermore, we observed that local treatment with blocking antibodies against IL-10 and CD36 on the day of surgery significantly inhibited lesion development. NP exposure also altered the estrous cycle in mice. The results suggest that chronic and low-dose exposure to NP enhances endometriotic lesion growth by altering pDC homeostasis and function. This study has important implications for understanding the environment-innate immunity interaction in human endometriosis.

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Condition tags

mesh:D004715endometriosis

MeSH descriptors

Endometriosis Phenols Animals Blotting, Western CD36 Antigens CD36 Antigens Dendritic Cells Dendritic Cells Dendritic Cells Endocrine Disruptors Endocrine Disruptors Endometriosis Female Flow Cytometry Humans Interleukin-10 Interleukin-10 Mice Mice, Inbred C57BL Phenols

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