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Updated: Jan 2, 2026
Murine Model of Allergen Induced Asthma
Published on: May 14, 2012
Oral exposure to low dose bisphenol A aggravates allergic airway inflammation in mice
Rie Yanagisawa1, Eiko Koike1, Tin-Tin Win-Shwe1
1Center for Health and Environmental Risk Research, National Institute for Environmental Studies, Tsukuba, Japan.
Abstract:
Bisphenol A (BPA) is widely used in many consumer products and has adverse effects on human health including allergic diseases. We investigated the effects of low dose BPA, comparable to actual human oral exposure, on allergic asthma in mice. C3H/HeJ male mice were fed a chow diet containing BPA (equivalent to 0.09, 0.90, or 9.01 μg/kg/day) and were intratracheally administered ovalbumin (OVA, 1 μg/animal) every two weeks from 5-11 weeks of age. All doses of BPA plus OVA enhanced pulmonary inflammation and airway hyperresponsiveness, and increased lung mRNA levels of Th2 cytokine/chemokine, and serum OVA-specific IgE and IgG1 compared to OVA alone, with greater effects observed in the middle- and high-dose BPA plus OVA groups. Furthermore, high-dose BPA with OVA decreased lung mRNA levels of ERβ and AR compared with OVA. Furthermore, BPA enhanced OVA-restimulated cell proliferation and protein levels of IL-4 and IL-5 in mediastinal lymph node (MLN) cells in OVA-sensitized mice. In bone marrow (BM) cells, middle-dose BPA with OVA increased Gr-1 expression. In conclusion, oral exposure to low-dose BPA at levels equivalent to human exposure can aggravate allergic asthmatic responses through enhancement of Th2-skewed responses, lung hormone receptor downregulation, and MLN and BM microenvironment change.
Insights
Low-dose Bisphenol A (BPA) exposure, similar to human levels, worsened allergic asthma in mice. BPA aggravated lung inflammation and airway hyperresponsiveness by enhancing Th2 responses and altering hormone receptor expression.
Area of Science:
- Environmental Health
- Toxicology
- Immunology
Background:
- Bisphenol A (BPA) is a ubiquitous chemical found in consumer products.
- BPA exposure is linked to adverse health outcomes, including allergic diseases.
- Understanding BPA's impact on allergic asthma at low, human-relevant doses is crucial.
Purpose of the Study:
- To investigate the effects of low-dose Bisphenol A (BPA) on allergic asthma.
- To determine if human oral exposure levels of BPA exacerbate asthma symptoms in a mouse model.
Main Methods:
- C3H/HeJ male mice were exposed to varying doses of BPA (0.09, 0.90, 9.01 μg/kg/day) via diet.
- Mice were sensitized and challenged with ovalbumin (OVA) to induce allergic asthma.
- Pulmonary inflammation, airway hyperresponsiveness, Th2 cytokine levels, IgE/IgG1, hormone receptor expression, and immune cell responses were assessed.
Main Results:
- All BPA doses combined with OVA enhanced pulmonary inflammation and airway hyperresponsiveness compared to OVA alone.
- BPA exposure increased Th2 cytokine/chemokine mRNA, serum OVA-specific IgE and IgG1.
- High-dose BPA reduced lung mRNA levels of estrogen receptor beta (ERβ) and androgen receptor (AR); BPA also modulated immune cell proliferation and cytokine production in mediastinal lymph nodes and bone marrow.
Conclusions:
- Oral exposure to low-dose BPA, comparable to human intake, aggravates allergic asthma.
- BPA exacerbates asthma by enhancing Th2-skewed immune responses.
- Mechanisms include lung hormone receptor downregulation and alterations in mediastinal lymph node and bone marrow microenvironments.
