Angiotensin II Type 1a–Deficient Bone Marrow–Derived Dendritic Cells Produce Higher Levels of Monocyte Chemoattractant Protein 1

Abstract

Recruitment of leukocytes plays a crucial role in the progression to irreversible damage in inflammatory states, such as cardiovascular and kidney diseases. Increased expression of MCP-1 is a critical link between angiotensin II and target organ inflammation. Dendritic cells (DCs) are highly specialized antigen-presenting cells with the ability to activate resting T lymphocytes and to initiate primary immune responses. We studied the production of cytokines by bone marrow–derived DCs deficient in AT1aR, AT1bR, or in both AT1 receptors. In line with the reports by Crowley et al,1,3 we found that DCs derived from AT1a KO and double KO mice released significantly higher levels of MCP-1 when compared with control mice. The difference remained significant even after stimulation with lipopolysaccharides. In contrast, no differences in the production of interleukin 10 and interleukin 12p70 were found between AT1KO-DC and WT-DC.1aR, AT1bR, or in both AT1 receptors. In line with the reports by Crowley et al,1,3 we found that DCs derived from AT1a KO and double KO mice released significantly higher levels of MCP-1 when compared with control mice. The difference remained significant even after stimulation with lipopolysaccharides. In contrast, no differences in the production of interleukin 10 and interleukin 12p70 were found between AT1KO-DC and WT-DC.1a KO and double KO mice released significantly higher levels of MCP-1 when compared with control mice. The difference remained significant even after stimulation with lipopolysaccharides. In contrast, no differences in the production of interleukin 10 and interleukin 12p70 were found between AT1KO-DC and WT-DC.1KO-DC and WT-DC.