Environmental estrogens induce mast cell degranulation and enhance IgE-mediated release of allergic mediators.
Open accessAbstract
BACKGROUND: Prevalence and morbidity of allergic diseases have increased over the last decades. Based on the recently recognized differences in asthma prevalence between the sexes, we have examined the effect of endogenous estrogens on a key element of the allergic response. Some lipophilic pollutants have estrogen-like activities and are termed environmental estrogens. These pollutants tend to degrade slowly in the environment and to bioaccumulate and bioconcentrate in the food chain; they also have long biological half-lives. OBJECTIVES: Our goal in this study was to identify possible pathogenic roles for environmental estrogens in the development of allergic diseases. METHODS: We screened a number of environmental estrogens for their ability to modulate the release of allergic mediators from mast cells. We incubated a human mast cell line and primary mast cell cultures derived from bone marrow of wild type and estrogen receptor alpha (ER-alpha)-deficient mice with environmental estrogens with and without estradiol or IgE and allergens. We assessed degranulation of mast cells by quantifying the release of beta-hexosaminidase. RESULTS: All of the environmental estrogens tested caused rapid, dose-related release of beta-hexosaminidase from mast cells and enhanced IgE-mediated release. The combination of physiologic concentrations of 17beta-estradiol and several concentrations of environmental estrogens had additive effects on mast cell degranulation. Comparison of bone marrow mast cells from ER-alpha-sufficient and ER-alpha-deficient mice indicated that much of the effect of environmental estrogens was mediated by ER-alpha. CONCLUSIONS: Our findings suggest that estrogenic environmental pollutants might promote allergic diseases by inducing and enhancing mast cell degranulation by physiologic estrogens and exposure to allergens.
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HMC-1 cells and BMMCs express both estradiol and progesterone receptors.
“As previously reported, HMC-1 and BMMCs express both, E2 and P4 receptors [27], [28], [24] (Fig. 3E–G).”
From Estradiol and Progesterone Regulate the Migration of Mast Cells from the Periphery to the Uterus and Induce Their Maturation and Degranulation (2010) · cites this paper as [28]
The Materials and Methods section describes HMC-1 cells and BMMCs, including BMMCs from estrogen receptor-α knockout mice; the Discussion also describes ER-α-dependent mast-cell responses. These passages support the estrogen-receptor portion, but the paper does not report progesterone-receptor expression in either cell type (searched: progesterone receptor, P4 receptor). No page numbers were available in our copy. (LLM, conf=0.85)
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- Authors
- Narita, S.-I., Goldblum, R. M., Watson, C. S., Brooks, E. G., Estes, D. M., Curran, E. M., & Midoro-Horiuti, T.
- Affiliations
- The University of Texas Medical Branch at Galveston (US)
- Department of Pediatrics, Child Health Research Center and
- ORCID
- Brooks, Edward G.
- Venue
- Environmental Health Perspectives
- Publisher
- American Chemical Society (ACS)
- Published
- 2006-10-03
- Volume
- 115
- Issue
- 1
- Pages
- 48-52
- ISSN
- 0091-6765 (ISSN-L)
- 1552-9924
- PMC
- PMC1797832
- OpenAlex
- W1989965047
- Cited by
- 186
- References
- 29
- Citations by year
- 2026: 6 · 2025: 10 · 2024: 6 · 2023: 7 · 2022: 9 · 2021: 9 · 2020: 7 · 2019: 12 · 2018: 9 · 2017: 8 · 2016: 11 · 2015: 17 · 2014: 10 · 2013: 9 · 2012: 14
- FWCI
- 2.52
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- public-domain
- creativecommons.org/licenses/by/4.0/ (vor, 4105 d)
- Locations
- Environmental Health Perspectives (publishedVersion, public-domain)
- Europe PMC (PubMed Central) (publishedVersion, public-domain)
- PubMed Central (publishedVersion, public-domain)
- PubMed (publishedVersion)
- Funders
- National Institute of Allergy and Infectious Diseases (R01AI052428, K08AI055792)
- National Institute of Environmental Health Sciences (R21ES016428)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Mast cells and histamine
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Effects and risks of endocrine disrupting chemicals
- Health Sciences › Medicine › Physiology › Asthma and respiratory diseases
- Keywords
- xenoestrogens, mast cell degranulation, IgE-mediated release, allergic mediators, estrogen receptor alpha, estradiol, allergic diseases, beta-hexosaminidase, endocrine disruptors, lipophilic pollutants, bone marrow mast cells, allergen exposure
- MeSH terms
- Animals, Aroclors, Asthma, Cell Line, Dichlorodiphenyl Dichloroethylene, Dieldrin, Dinitrophenols, Endosulfan, Environmental Pollutants, Estradiol, Estrogens, Non-Steroidal, Humans, Immunoglobulin E, Mast Cells, Mice, Inbred C57BL, Pesticides, Phenols, Serum Albumin, Bovine, Cell Degranulation, Mice, Knockout, Chlorodiphenyl (54% Chlorine), Antigens, Dermatophagoides, Estrogen Receptor alpha, Mice
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