| Summary: | 碩士 === 高雄醫學大學 === 醫學研究所-基礎醫學組 === 102 === Abstract
Introduction: Di (2-ethylhexyl) phthalate (DEHP) is widely used in plastic products such as polyvinyl chloride plastics. DEHP is not covalently bound to the plastic matrix, so DEHP exposure to the environment is easy, resulting in contamination of the external environment. Our previous studies found that maternal exposure to DEHP enhanced the severity of airway allergic inflammation in the offspring as compared to the control.
Aim: The dendritic cell (DC) plays an important role in the pathogenesis of asthma, therefore, the aim of this study is to clarify the effect of maternal DEHP exposure on DC homeostasis in F1 offspring.
Method: To simulate the ways in which humans are affected by exposure to DEHP, we established an asthma model of offspring after maternal exposure to DEHP and analyzed the percentages and numbers of splenic DCs and subsets in F1 offspring. We also observed DC precursors in bone marrow of offspring. Finally, we analyzed the apoptosis of DCs and DC precursors.
Result: After low-dose and long-term exposure to DEHP, the OVA-immunized F1 neonate mice were observed. We found that the percentage and numbers of splenic cDCs were significantly decreased in DEHP-exposed F1 neonates. In addition, the percentages of bone marrow DC precursors were also decreased in DEHP group. This may be due to the increased apoptotic rates of DC precursors in DEHP F1 offspring. We also found that percentage of the CD4+CD8－ DCs was increased and the percentage of CD4－CD8+ DCs was decreased in the DEHP F1 spleen. In the immunized adult DEHP F1 mice, the percentage and cell number of splenic cDCs were also decreased. Although the percentage of DC precursors was not different in these two groups, the percentage of B220+ cells in DC precursors was increased in DEHP group. We also found that the percentage of apoptotic DC precursors was increased, the percentage of CD4+CD8－ DCs was also increased and the percentage of CD4－CD8－ DCs was decreased in DEHP F1 offspring.
Conclusion: These results indicate that maternal exposure to DEHP may influence the DC homeostasis and enhance the severity of allergic lung inflammation in the F1 offspring.
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