Aryl hydrocarbon receptor activation increases α4β7 integrin expression on RAW 264.7 mouse macrophage cells 2672

Abstract Description The aryl hydrocarbon receptor (AhR) plays an essential role in immunoregulation. Chemokine receptor 9 (CCR9) and integrin α4β7 are migratory markers that are integral for immune cell homing to the gut. AhR activation has been shown to enhance the migration of some CD4+ T cells to the gut of mice. Our laboratory has additionally demonstrated that AhR activation can significantly enhance CCR9 and integrin α4β7 expression on activated primary mouse B cells in vitro. In this study, we hypothesized that AhR activation would similarly enhance the expression of intestinal migration markers on RAW 264.7 mouse macrophage cells. To test this hypothesis, RAW 264.7 cells were exposed to CH22319 (AhR antagonist, 20 µM) or FICZ (AhR agonist, 40 µM) for 48 hours in culture after which the expression of CCR9 and integrin α4β7 was determined by flow cytometry. We found that AhR agonist exposure significantly increased the fraction of RAW 264.7 cells expressing integrin α4β7, relative to the AhR antagonist-exposed cells, from 51% to 61% (P < 0.05), whereas CCR9 was expressed on all RAW 264.7 cells and AhR ligand exposure did not alter that. In contrast to activated B cells, AhR activation did not significantly alter the level of expression (MFI) of either CCR9 or LPAM-1 on RAW 264.7 cells. These results suggest that enhanced migration to the gut may be a common modification of immune cell behavior following AhR activation. Funding Sources Supported by University of Northern Colorado’s Office of Undergraduate Research; Beta Beta Beta Biological Honor Society Topic Categories Cellular Adhesion, Migration, and Inflammation (CAM)