Inhaled Fine Particles Induce Alveolar Macrophage Death and Interleukin-1α Release to Promote Inducible Bronchus-Associated Lymphoid Tissue Formation

Publication date: 20 December 2016
Source:Immunity, Volume 45, Issue 6
Author(s): Etsushi Kuroda, Koji Ozasa, Burcu Temizoz, Keiichi Ohata, Christine X. Koo, Tomohiro Kanuma, Takato Kusakabe, Shingo Kobari, Masanori Horie, Yasuo Morimoto, Saeko Nakajima, Kenji Kabashima, Steven F. Ziegler, Yoichiro Iwakura, Wataru Ise, Tomohiro Kurosaki, Takahiro Nagatake, Jun Kunisawa, Naoki Takemura, Satoshi Uematsu, Masayuki Hayashi, Taiki Aoshi, Kouji Kobiyama, Cevayir Coban, Ken J. Ishii
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-1α (IL-1α) and caused inducible bronchus-associated lymphoid tissue (iBALT) formation in the lung. IL-1α 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-1α release and iBALT formation, even long after particulate instillation. Recombinant IL-1α 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-1α-iBALT axis might be a therapeutic target for particulate-induced allergic inflammation.

Graphical abstract

Teaser

Inhaled fine particulates are known to induce allergic responses, but the exact cell types and immunological factors that initiate the lung-specific immune responses remain unclear. Kuroda et al. (2016) show that particulates trigger tertiary lymphoid organ formation in the lung as a consequence of alveolar macrophage death and IL-1α release.


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