Phthalate Exposure During the Prenatal and Lactational Period Increases the Susceptibility to Rheumatoid Arthritis in Mice

被引:14
|
作者
Elter, Elena [1 ,2 ]
Wagner, Marita [1 ,2 ]
Buchenauer, Lisa [1 ,2 ]
Bauer, Mario [1 ]
Polte, Tobias [1 ,2 ]
机构
[1] UFZ Helmholtz Ctr Environm Res Leipzig Halle, Dept Environm Immunol, Leipzig, Germany
[2] Univ Leipzig, Med Ctr, Dept Dermatol Venerol & Allergol, Leipzig, Germany
来源
FRONTIERS IN IMMUNOLOGY | 2020年 / 11卷
关键词
perinatal exposure; rheumatoid arthritis; phthalates; early programming; autoimmune disease; COLLAGEN-INDUCED ARTHRITIS; ASTHMA; EXPRESSION; AUTOIMMUNITY; RECEPTOR;
D O I
10.3389/fimmu.2020.00550
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The prenatal and early postnatal period is highly sensitive to environmental exposures that may interfere with the developmental programming of the immune system leading to an altered disease risk in later life. To clarify the role of early influences in activation or exacerbation of autoimmune diseases like rheumatoid arthritis (RA) we investigated the effect of maternal exposure during the prenatal and lactational period of DBA/1 mice to the plasticizer benzyl butyl phthalate (BBP) on the development of RA in the offspring. Using a mild collagen-induced arthritis (CIA) model, maternal BBP-exposure increased both the prevalence and the severity of RA in the progeny compared to un-exposed dams. Additionally, maternal BBP exposure led to elevated serum IgG(1) and IgG(2a) level in the offspring and increased the IFN-gamma and IL-17 release from collagen-re-stimulated spleen cells. Transcriptome analysis of splenocytes isolated from 3-week-old pups before RA-induction revealed considerable changes in gene expression in the offspring from BBP-exposed dams. Among them were regulator of G-protein signaling 1 (rgs1), interleukin-7 receptor (il-7r) and CXC chemokine 4 (cxcr4), all genes that have previously been described as associated with RA pathology. In summary, our results demonstrate that perinatal exposure to BBP increases the susceptibility of the offspring to RA, probably via a phthalate-induced disturbed regulation of RA-relevant genes or signaling pathways.
引用
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页数:10
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