T-helper type-2 contact hypersensitivity of Balb/c mice aggravated by dibutyl phthalate via long-term dermal exposure.
OBJECTIVE
During the last few decades, the prevalence of allergic skin diseases, asthma and rhinitis, has increased worldwide. Introduction of environmental chemicals with aggravation effects may play a part in this increase. The artificial chemical product dibutyl phthalate (DBP) is used in many products used in daily life. Dermal exposure to DBP is a common (but easily neglected) exposure pattern.


RESULTS
In this study, we examined the aggravation effect of long-term dermal exposure to DBP in a T-helper type 2 (Th2) model of contact hypersensitivity (CHS) in mice, and sought the potential molecular mechanisms. Experimental tests were conducted after 40-day dermal exposure to saline or three concentrations of DBP and subsequent three times of sensitization with 0.5% fluorescein isothiocyanate (FITC) or vehicle. The results of immunological and inflammatory biomarkers (total-immunoglobulin (Ig)E and Th cytokines) as well as histopathological examination and measurement of ear swelling supported the notion that high doses of DBP may promote and aggravate atopic dermatitis. Increased expression of thymic stromal lymphopoietin (TSLP) in this mouse model suggested that TSLP might be one of the molecular mechanisms of the aggravation effect induced by DBP.


CONCLUSIONS
Together, these results indicated that long-term dermal exposure to types of environmental toxins such as phthalates may endow an atopic predisposition in animals or humans. In addition, the high expression of TSLP in the mouse model demonstrated that TSLP might have an important role in the aggravation effect. This result could help to provide effective prevention strategies against atopic diseases such as atopic dermatitis (AD).
Section of Environmental Biomedicine, Hubei Key Laboratory of Genetic Regulation and Integrative Biology, College of Life Sciences, Central China Normal University, Wuhan, China.
Jinquan
J
Li
Section of Environmental Biomedicine, Hubei Key Laboratory of Genetic Regulation and Integrative Biology, College of Life Sciences, Central China Normal University, Wuhan, China.
Li
L
Li
Section of Environmental Biomedicine, Hubei Key Laboratory of Genetic Regulation and Integrative Biology, College of Life Sciences, Central China Normal University, Wuhan, China.
Haoxiao
H
Zuo
Section of Environmental Biomedicine, Hubei Key Laboratory of Genetic Regulation and Integrative Biology, College of Life Sciences, Central China Normal University, Wuhan, China.
Chenjuan
C
Ke
Section of Environmental Biomedicine, Hubei Key Laboratory of Genetic Regulation and Integrative Biology, College of Life Sciences, Central China Normal University, Wuhan, China.
Biao
B
Yan
Section of Environmental Biomedicine, Hubei Key Laboratory of Genetic Regulation and Integrative Biology, College of Life Sciences, Central China Normal University, Wuhan, China.
Huaxiao
H
Wen
Department of Building Science, Tsinghua University, Beijing, China.
Yinping
Y
Zhang
Section of Environmental Biomedicine, Hubei Key Laboratory of Genetic Regulation and Integrative Biology, College of Life Sciences, Central China Normal University, Wuhan, China.
Xu
X
Yang
D000818:Animals; D003877:Dermatitis, Contact / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D020405:Dermis / Q000187:drug effects / Q000276:immunology* / Q000473:pathology; D003993:Dibutyl Phthalate / Q000494:pharmacology*; D004797:Enzyme-Linked Immunosorbent Assay; D007124:Immunoenzyme Techniques; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D010968:Plasticizers / Q000494:pharmacology; D012871:Skin Diseases / Q000139:chemically induced / Q000276:immunology* / Q000473:pathology; D018418:Th2 Cells / Q000187:drug effects / Q000276:immunology* / Q000473:pathology; D013997:Time Factors
D010968:Plasticizers; D003993:Dibutyl Phthalate