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Immunity. 2016 Dec 20;45(6):1299-1310. doi: 10.1016/j.immuni.2016.11.010.

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

Author information

1
Laboratory of Vaccine Science, WPI Immunology Frontier Research Center, Osaka University, Osaka 565-0871, Japan; Laboratory of Vaccine Design, Center for Drug Design Research, National Institutes of Biomedical Innovation, Health and Nutrition, Osaka 567-0085, Japan; Laboratory of Adjuvant Innovation, National Institutes of Biomedical Innovation, Health and Nutrition, Osaka 567-0085, Japan. Electronic address: kuroetu@ifrec.osaka-u.ac.jp.
2
Laboratory of Adjuvant Innovation, National Institutes of Biomedical Innovation, Health and Nutrition, Osaka 567-0085, Japan; Department of Pediatrics, Yokohama City University Graduate School of Medicine, Kanagawa 236-0004, Japan.
3
Laboratory of Vaccine Science, WPI Immunology Frontier Research Center, Osaka University, Osaka 565-0871, Japan.
4
Laboratory of Adjuvant Innovation, National Institutes of Biomedical Innovation, Health and Nutrition, Osaka 567-0085, Japan; Immunology Programme and Department of Microbiology, Centre for Life Science, National University of Singapore 117456, Singapore; NUS Graduate School of Integrated Sciences & Engineering, National University of Singapore 117456, Singapore.
5
Laboratory of Vaccine Science, WPI Immunology Frontier Research Center, Osaka University, Osaka 565-0871, Japan; Laboratory of Adjuvant Innovation, National Institutes of Biomedical Innovation, Health and Nutrition, Osaka 567-0085, Japan.
6
Health Research Institute, National Institute of Advanced Industrial Science and Technology, Kagawa 761-0395, Japan.
7
Department of Occupational Pneumology, University of Occupational and Environmental Health, Japan, Fukuoka 807-8555, Japan.
8
Department of Dermatology, Kyoto University, Graduate School of Medicine, Kyoto 606-8317, Japan.
9
Immunology Program, Benaroya Research Institute, Seattle, WA 98101-2795, USA.
10
Research Institute for Biomedical Science, Tokyo University of Science, Chiba 278-0222, Japan.
11
Laboratory of Lymphocyte Differentiation, WPI Immunology Frontier Research Center, Osaka University, Osaka 565-0871, Japan.
12
Vaccine Materials, National Institutes of Biomedical Innovation, Health and Nutrition, Osaka 567-0085, Japan.
13
Department of Mucosal Immunology, School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba 260-8670, Japan; Division of Innate Immune Regulation, International Research and Development Center for Mucosal Vaccines, Institute of Medical Science, The University of Tokyo, 4-6-1 Shirokanedai, Minato-ku, Tokyo 108-8639, Japan.
14
Laboratory of Vaccine Science, WPI Immunology Frontier Research Center, Osaka University, Osaka 565-0871, Japan; Laboratory of Adjuvant Innovation, National Institutes of Biomedical Innovation, Health and Nutrition, Osaka 567-0085, Japan; Vaccine Research Development Office, Advanced Drug Research Laboratories, Sohyaku. Innovative Research Division, Mitsubishi Tanabe Pharma Corporation, Kanagawa 227-0033, Japan.
15
Laboratory of Adjuvant Innovation, National Institutes of Biomedical Innovation, Health and Nutrition, Osaka 567-0085, Japan; Vaccine Dynamics Project, BIKEN Innovative Vaccine Research Alliance Laboratories, Research Institute for Microbial Diseases, Osaka, 565-0871, Japan.
16
Laboratory of Vaccine Science, WPI Immunology Frontier Research Center, Osaka University, Osaka 565-0871, Japan; Laboratory of Adjuvant Innovation, National Institutes of Biomedical Innovation, Health and Nutrition, Osaka 567-0085, Japan; La Jolla Institute for Allergy and Immunology, La Jolla, CA, 92037, USA.
17
Laboratory of Malaria Immunology, WPI Immunology Frontier Research Center, Osaka University, Osaka 565-0871, Japan.
18
Laboratory of Vaccine Science, WPI Immunology Frontier Research Center, Osaka University, Osaka 565-0871, Japan; Laboratory of Vaccine Design, Center for Drug Design Research, National Institutes of Biomedical Innovation, Health and Nutrition, Osaka 567-0085, Japan; Laboratory of Adjuvant Innovation, National Institutes of Biomedical Innovation, Health and Nutrition, Osaka 567-0085, Japan. Electronic address: kenishii@biken.osaka-u.ac.jp.

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.

KEYWORDS:

IL-1α; IgE; Particulate; alveolar macrophages; iBALT

PMID:
28002730
DOI:
10.1016/j.immuni.2016.11.010
[Indexed for MEDLINE]
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