| Summary: | 碩士 === 高雄醫學大學 === 生物科技學系碩士班 === 100 === Abstract
Ubiquitous environmental contaminants such as benzopyrene, polychlorinated biphenyls, dioxin-like compounds 2,3,7,8-Tetrachlorodibenzo-p-dioxin in air and cigarette smoke recently are linked to immune regulation. These noxious agents are well known as aryl hydrocarbon receptor (AhR) ligand-activated transcription factors. AhR plays an important role in gene alteration, cell-cell adhesion, cytokine expression, and mucin production, which are involved in the induction of cancer or inflammation. Previous study also indicated that TCDD is involved in immune regulation and is associated with disruption of the immune system. In the study, we investigated how TCDD affect monocytes differentiated to M1/M2 macrophages. We first treated THP-1 with TCDD to examine whether TCDD can induce THP-1 differentiation into M1- or M2-polarized macrophage. We found that TCDD did not change cytokine expression of THP-1. However, following, we treated THP-1 with TCDD during and after its differentiation. Our results showed that TCDD increases CCL1 expression during M2-polarized differentiation. Moreover, chromatin immunoprecipitation assay indicated that there are two XRE motifs, which located at -312 bp and -2803 bp of CCL1 promoter during M2 macrophage differentiation. However, only one XRE motif located at -312 bp in M1 macrophage differentiation. Thus, the study provided a novel mechanism of CCL1 gene regulation during M1- and M2-polarized macrophage under TCDD exposure.
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