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

Abstract：

: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.

journal_name

Immunity

journal_title

Immunity

authors

Kuroda E,Ozasa K,Temizoz B,Ohata K,Koo CX,Kanuma T,Kusakabe T,Kobari S,Horie M,Morimoto Y,Nakajima S,Kabashima K,Ziegler SF,Iwakura Y,Ise W,Kurosaki T,Nagatake T,Kunisawa J,Takemura N,Uematsu S,Hayashi M,Aoshi T

doi

10.1016/j.immuni.2016.11.010

subject

Has Abstract

pub_date

2016-12-20 00:00:00

pages

1299-1310

issue

6

eissn

1074-7613

issn

1097-4180

pii

S1074-7613(16)30482-4

journal_volume

45

pub_type

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