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RAGE signaling influences diesel particulate matter‐induced inflammation in primary alveolar macrophages

Receptors for advanced glycation end‐products (RAGE) are members of the immunoglobulin superfamily of cell‐surface receptors implicated in pulmonary inflammation. In the present study, we tested the hypothesis that RAGE mediates inflammation in primary alveolar macrophages (AMs) triggered by diesel particulate matter (DPM). Using real time RT‐PCR, we discovered that RAGE was up‐regulated in primary AMs exposed to DPM for four hours. Because DPM increased RAGE expression, we exposed primary AMs isolated from RAGE null and wild type Balb/C mice to DPM. DPM led to the activation p38 and NF‐kB and that these two signaling intermediates were diminished in similarly exposed AMs isolated from RAGE null mice. Furthermore, TNF‐a, IL‐12, and IL‐13 were all significantly decreased in culture media from DPM‐exposed RAGE null AMs compared to similarly exposed WT AMs. These results demonstrate that primary AMs orchestrate diesel‐induced inflammation, at least in part, via RAGE‐mediated mechanisms. Further work may show that RAGE signaling is a potential target in treatment of inflammatory lung diseases exacerbated by environmental pollution. This work was supported by a grant from the Flight Attendant's Medical Research Institute (FAMRI, PRR) and a BYU Mentoring Environment Grant (PRR).