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Pulmonary toxicity and adjuvant effect of di-(2-exylhexyl) phthalate in ovalbumin-immunized BALB/c mice
Hubei Key Laboratory of Genetic Regulation and Integrative Biology, Huazhong Normal University, Wuhan, China.
Hubei Key Laboratory of Genetic Regulation and Integrative Biology, Huazhong Normal University, Wuhan, China.
Hubei Key Laboratory of Genetic Regulation and Integrative Biology, Huazhong Normal University, Wuhan, China.
Hubei Key Laboratory of Genetic Regulation and Integrative Biology, Huazhong Normal University, Wuhan, China.
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2012 (English)In: PLoS ONE, E-ISSN 1932-6203, Vol. 7, no 6, article id e39008Article in journal (Refereed) Published
Abstract [en]

BACKGROUND: Asthma is a complex pulmonary inflammatory disease, which is characterized by airway hyperresponsiveness, variable airflow obstruction and inflammation in the airways. The majority of asthma is allergic asthma, which is a disease caused by type I hypersensitivity mediated by IgE. Exposures to a number of environmental chemicals are suspected to lead to asthma, one such pollutant is di-(2-ethylheyl) phthalate (DEHP). DEHP is a manufactured chemical that is commonly added in plastic products to make them flexible. Epidemiological studies have revealed a positive association between DEHP exposure and asthma prevalence.

METHODOLOGY/PRINCIPAL FINDINGS: The present study was aimed to determine the underlying role of DEHP exposure in airway reactivity, especially when combined with allergen exposure. The biomarkers include pulmonary histopathology, airway hyperresponsiveness (lung function), IgE, IL-4, IFN-γ and eosinophils. Healthy balb/c mice were randomly divided into eight exposure groups (n = 8 each): (1) saline control, (2) 30 µg/(kg•d) DEHP, (3) 300 µg/(kg•d) DEHP, (4) 3000 µg/(kg•d) DEHP, and (5) ovalbumin (OVA)-sensitized group, (6) OVA-combined with 30 µg/(kg•d) DEHP, (7) OVA-combined with 300 µg/(kg•d) DEHP, and (8) OVA-combined with 3000 µg/(kg•d) DEHP. Experimental tests were conducted after 52-day DEHP exposure and subsequently one week of challenge with aerosolized OVA. The principal findings include: (1) Strong postive associations exist between OVA-combined DEHP exposure and serum total IgE (T-IgE), as well as histological findings. These positive associations show a dose-dependent low dose sensitive effect of DEHP. (2) IL-4, eosinophil recruitment and lung function are also indicators for adjuvant effect of DEHP.

CONCLUSIONS/SIGNIFICANCE: Our results suggest that except the significant changes of immunological and inflammatory biomarkers (T-IgE, IL-4, IFN-γ and eosinophils), the pulmonary histological (histopathological examination) and physiological (lung function) data also support that DEHP may promote and aggravate allergic asthma by adjuvant effect.

Place, publisher, year, edition, pages
PLOS , 2012. Vol. 7, no 6, article id e39008
National Category
Respiratory Medicine and Allergy
Research subject
Biomedical Science
Identifiers
URN: urn:nbn:se:oru:diva-79032DOI: 10.1371/journal.pone.0039008ISI: 000305340000059PubMedID: 22701742Scopus ID: 2-s2.0-84862224204OAI: oai:DiVA.org:oru-79032DiVA, id: diva2:1386332
Note

This work was supported by the China National Natural Science Foundation (grant ID: 51136002, 51076079) and National Key Technologies R&D Program of China (grant ID: 2012BAJ02B03). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Available from: 2013-10-17 Created: 2020-01-17 Last updated: 2020-01-28Bibliographically approved

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Nånberg, EewaBornehag, Carl-Gustaf

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