| First Author | Kuroda E | Year | 2016 |
| Journal | Immunity | Volume | 45 |
| Issue | 6 | Pages | 1299-1310 |
| PubMed ID | 28002730 | Mgi Jnum | J:291647 |
| Mgi Id | MGI:6141368 | Doi | 10.1016/j.immuni.2016.11.010 |
| Citation | Kuroda E, et al. (2016) Inhaled Fine Particles Induce Alveolar Macrophage Death and Interleukin-1alpha Release to Promote Inducible Bronchus-Associated Lymphoid Tissue Formation. Immunity 45(6):1299-1310 |
| abstractText | Particulate pollution is thought to function as an adjuvant that can induce allergic responses. However, the exact cell types and immunological factors that initiate the lung-specific immune responses are unclear. We found that upon intratracheal instillation, particulates such as aluminum salts and silica killed alveolar macrophages (AMs), which then released interleukin-1alpha (IL-1alpha) and caused inducible bronchus-associated lymphoid tissue (iBALT) formation in the lung. IL-1alpha release continued for up to 2 weeks after particulate exposure, and type-2 allergic immune responses were induced by the inhalation of antigen during IL-1alpha release and iBALT formation, even long after particulate instillation. Recombinant IL-1alpha was sufficient to induce iBALTs, which coincided with subsequent immunoglobulin E responses, and IL-1-receptor-deficient mice failed to induce iBALT formation. Therefore, the AM-IL-1alpha-iBALT axis might be a therapeutic target for particulate-induced allergic inflammation. |
