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The chemokine CCL20, the unique ligand of CCR6 functions as an attractant of immune cells. Expression of CCL20 is induced by Toll-like Receptor (TLR) signaling or proinflammatory cytokine stimulation. However CCL20 is also constitutively produced at specific epithelial sites of mucosa. This expression profile is achieved by transcriptional regulation. In the present work we characterized regulatory features of mouse  Ccl20  gene. Transcriptional fusions between the mouse  Ccl20  promoter and the firefly luciferase ( luc ) encoding gene were constructed and assessed in  in vitro  and  in vivo  assays. We found that liver CCL20 expression and luciferase activity were upregulated by systemic administration of the TLR5 agonist flagellin. Using shRNA and dominant negative form specific for mouse TLR5, we showed that this expression was controlled by TLR5. To address  in situ  the regulation of gene activity, a transgenic mouse line harboring a functional  Ccl20-luc  fusion was generated. The luciferase expression was highly concordant with  Ccl20  expression in different tissues. Our data indicate that the transgenic mouse model can be used to monitor activation of innate response  in vivo .

Transgenic Mouse Model Harboring the Transcriptional Fusion Ccl20-Luciferase as a Novel Reporter of Pro-Inflammatory Response