Abstract
Receptors for advanced glycation end‐products (RAGE) are members of an immunoglobin superfamily of cell‐surface receptors expressed in alveolar type I (ATI) epithelial cells. RAGE has also been implicated in mechanisms of sustained pulmonary inflammation. In the present study, we test the hypothesis that diesel particulate matter (DPM) up‐regulates RAGE in rat ATI‐like R3/1 cells and induces an inflammatory response. Using real time RT‐PCR and immunoblotting, we demonstrate that RAGE mRNA and protein are up‐regulated in R3/1 cells exposed to DPM. Immunostaining and reporter gene assays revealed increased nuclear translocation and activity of NF‐kB in DPM‐exposed R3/1 cells when compared to cells transfected with small interfering RNA for RAGE (siRAGE) prior to DPM exposure. Lastly, ELISA revealed that two inflammatory cytokines, MCP‐1 and Il‐8, were significantly decreased in DPM‐exposed R3/1 cells that incorporated siRAGE when compared to cells without siRAGE. These data offer novel insights into potential mechanisms whereby RAGE influences pulmonary inflammation exacerbated by DPM exposure. Further research may demonstrate that molecules involved in RAGE signaling are potential targets in the successful pharmacological treatment of inflammatory lung diseases. Supported by the Flight Attendants Medical Research Institute (FAMRI, PRR) and BYU MEG Award (PRR).
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