Acceleration of acute lung inflammation by IL-1α released through cell death of alveolar macrophages upon phagocytosis of fine Asian sand dust particles
[Display omitted] •The study uses fine Asian sand dust particles, with a high impact on the lungs.•Asian sand dust is rapidly phagocytosed by alveolar macrophages.•Cell death of alveolar macrophages results in the release of IL-1α.•IL-1α is a critical mediator in the initiation of acute lung inflamm...
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Published in | Environment international Vol. 194; p. 109178 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Netherlands
Elsevier Ltd
01.12.2024
Elsevier |
Subjects | |
Online Access | Get full text |
ISSN | 0160-4120 1873-6750 1873-6750 |
DOI | 10.1016/j.envint.2024.109178 |
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Abstract | [Display omitted]
•The study uses fine Asian sand dust particles, with a high impact on the lungs.•Asian sand dust is rapidly phagocytosed by alveolar macrophages.•Cell death of alveolar macrophages results in the release of IL-1α.•IL-1α is a critical mediator in the initiation of acute lung inflammation.•Endotoxin in Asian sand dust was found to be involved in the release of IL-1α.
Asian sand dust (ASD), a significant desert sand dust, contains sub-2.5 µm fine particles and adversely affects human health, particularly exacerbating respiratory diseases. Despite this, the intricate physiological responses triggered by inhaled ASD particles remain incompletely understood. This study aimed to comprehensively examine the respiratory effects of ASD, focusing on the spatial distribution of inhaled ASD fine particles within the lungs and the immediate physiological responses they incite. Intratracheal administration of ASD fine particles in mice resulted in efficient phagocytosis by alveolar macrophages (AMs), leading to subsequent neutrophilic inflammation. A subset of ASD-phagocytosed AMs underwent necroptosis, releasing interleukin-1α (IL-1α), causing an increase in chemokines and neutrophils. These responses occurred rapidly within hours of exposure, with endotoxin in ASD particles contributing to the process. Despite variations in desert sand dust composition based on collection locale and timing, this study’s findings provide a foundational basis for understanding the biological effects of desert sand dust. Insights gained into the biological responses to desert sand dust hold promise for developing preventive measures such as air purifiers, and therapeutic agents such as IL-1α neutralizing antibodies, antibacterial agents and cell death inhibitors for human diseases associated with such environmental exposures. |
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AbstractList | [Display omitted]
•The study uses fine Asian sand dust particles, with a high impact on the lungs.•Asian sand dust is rapidly phagocytosed by alveolar macrophages.•Cell death of alveolar macrophages results in the release of IL-1α.•IL-1α is a critical mediator in the initiation of acute lung inflammation.•Endotoxin in Asian sand dust was found to be involved in the release of IL-1α.
Asian sand dust (ASD), a significant desert sand dust, contains sub-2.5 µm fine particles and adversely affects human health, particularly exacerbating respiratory diseases. Despite this, the intricate physiological responses triggered by inhaled ASD particles remain incompletely understood. This study aimed to comprehensively examine the respiratory effects of ASD, focusing on the spatial distribution of inhaled ASD fine particles within the lungs and the immediate physiological responses they incite. Intratracheal administration of ASD fine particles in mice resulted in efficient phagocytosis by alveolar macrophages (AMs), leading to subsequent neutrophilic inflammation. A subset of ASD-phagocytosed AMs underwent necroptosis, releasing interleukin-1α (IL-1α), causing an increase in chemokines and neutrophils. These responses occurred rapidly within hours of exposure, with endotoxin in ASD particles contributing to the process. Despite variations in desert sand dust composition based on collection locale and timing, this study’s findings provide a foundational basis for understanding the biological effects of desert sand dust. Insights gained into the biological responses to desert sand dust hold promise for developing preventive measures such as air purifiers, and therapeutic agents such as IL-1α neutralizing antibodies, antibacterial agents and cell death inhibitors for human diseases associated with such environmental exposures. Asian sand dust (ASD), a significant desert sand dust, contains sub-2.5 µm fine particles and adversely affects human health, particularly exacerbating respiratory diseases. Despite this, the intricate physiological responses triggered by inhaled ASD particles remain incompletely understood. This study aimed to comprehensively examine the respiratory effects of ASD, focusing on the spatial distribution of inhaled ASD fine particles within the lungs and the immediate physiological responses they incite. Intratracheal administration of ASD fine particles in mice resulted in efficient phagocytosis by alveolar macrophages (AMs), leading to subsequent neutrophilic inflammation. A subset of ASD-phagocytosed AMs underwent necroptosis, releasing interleukin-1α (IL-1α), causing an increase in chemokines and neutrophils. These responses occurred rapidly within hours of exposure, with endotoxin in ASD particles contributing to the process. Despite variations in desert sand dust composition based on collection locale and timing, this study's findings provide a foundational basis for understanding the biological effects of desert sand dust. Insights gained into the biological responses to desert sand dust hold promise for developing preventive measures such as air purifiers, and therapeutic agents such as IL-1α neutralizing antibodies, antibacterial agents and cell death inhibitors for human diseases associated with such environmental exposures. Asian sand dust (ASD), a significant desert sand dust, contains sub-2.5 µm fine particles and adversely affects human health, particularly exacerbating respiratory diseases. Despite this, the intricate physiological responses triggered by inhaled ASD particles remain incompletely understood. This study aimed to comprehensively examine the respiratory effects of ASD, focusing on the spatial distribution of inhaled ASD fine particles within the lungs and the immediate physiological responses they incite. Intratracheal administration of ASD fine particles in mice resulted in efficient phagocytosis by alveolar macrophages (AMs), leading to subsequent neutrophilic inflammation. A subset of ASD-phagocytosed AMs underwent necroptosis, releasing interleukin-1α (IL-1α), causing an increase in chemokines and neutrophils. These responses occurred rapidly within hours of exposure, with endotoxin in ASD particles contributing to the process. Despite variations in desert sand dust composition based on collection locale and timing, this study’s findings provide a foundational basis for understanding the biological effects of desert sand dust. Insights gained into the biological responses to desert sand dust hold promise for developing preventive measures such as air purifiers, and therapeutic agents such as IL-1α neutralizing antibodies, antibacterial agents and cell death inhibitors for human diseases associated with such environmental exposures. Asian sand dust (ASD), a significant desert sand dust, contains sub-2.5 µm fine particles and adversely affects human health, particularly exacerbating respiratory diseases. Despite this, the intricate physiological responses triggered by inhaled ASD particles remain incompletely understood. This study aimed to comprehensively examine the respiratory effects of ASD, focusing on the spatial distribution of inhaled ASD fine particles within the lungs and the immediate physiological responses they incite. Intratracheal administration of ASD fine particles in mice resulted in efficient phagocytosis by alveolar macrophages (AMs), leading to subsequent neutrophilic inflammation. A subset of ASD-phagocytosed AMs underwent necroptosis, releasing interleukin-1α (IL-1α), causing an increase in chemokines and neutrophils. These responses occurred rapidly within hours of exposure, with endotoxin in ASD particles contributing to the process. Despite variations in desert sand dust composition based on collection locale and timing, this study's findings provide a foundational basis for understanding the biological effects of desert sand dust. Insights gained into the biological responses to desert sand dust hold promise for developing preventive measures such as air purifiers, and therapeutic agents such as IL-1α neutralizing antibodies, antibacterial agents and cell death inhibitors for human diseases associated with such environmental exposures.Asian sand dust (ASD), a significant desert sand dust, contains sub-2.5 µm fine particles and adversely affects human health, particularly exacerbating respiratory diseases. Despite this, the intricate physiological responses triggered by inhaled ASD particles remain incompletely understood. This study aimed to comprehensively examine the respiratory effects of ASD, focusing on the spatial distribution of inhaled ASD fine particles within the lungs and the immediate physiological responses they incite. Intratracheal administration of ASD fine particles in mice resulted in efficient phagocytosis by alveolar macrophages (AMs), leading to subsequent neutrophilic inflammation. A subset of ASD-phagocytosed AMs underwent necroptosis, releasing interleukin-1α (IL-1α), causing an increase in chemokines and neutrophils. These responses occurred rapidly within hours of exposure, with endotoxin in ASD particles contributing to the process. Despite variations in desert sand dust composition based on collection locale and timing, this study's findings provide a foundational basis for understanding the biological effects of desert sand dust. Insights gained into the biological responses to desert sand dust hold promise for developing preventive measures such as air purifiers, and therapeutic agents such as IL-1α neutralizing antibodies, antibacterial agents and cell death inhibitors for human diseases associated with such environmental exposures. |
ArticleNumber | 109178 |
Author | Ishikawa, Raga Ichinose, Takamichi Honda, Akiko Miyasaka, Natsuko Kawahito, Yutaka Nagao, Megumi Takano, Hirohisa Sagawa, Tomoya Kuroda, Etsushi Okuda, Tomoaki |
Author_xml | – sequence: 1 givenname: Tomoya surname: Sagawa fullname: Sagawa, Tomoya email: t-sagawa@koto.kpu-m.ac.jp organization: Graduate School of Global Environmental Studies, Kyoto University, Kyoto, Japan – sequence: 2 givenname: Takamichi surname: Ichinose fullname: Ichinose, Takamichi organization: Graduate School of Global Environmental Studies, Kyoto University, Kyoto, Japan – sequence: 3 givenname: Akiko surname: Honda fullname: Honda, Akiko organization: Department of Environmental Engineering, Graduate School of Engineering, Kyoto University, Kyoto, Japan – sequence: 4 givenname: Etsushi surname: Kuroda fullname: Kuroda, Etsushi organization: Department of Immunology, School of Medicine, Hyogo Medical University, Hyogo, Japan – sequence: 5 givenname: Raga surname: Ishikawa fullname: Ishikawa, Raga organization: Graduate School of Global Environmental Studies, Kyoto University, Kyoto, Japan – sequence: 6 givenname: Natsuko surname: Miyasaka fullname: Miyasaka, Natsuko organization: Graduate School of Global Environmental Studies, Kyoto University, Kyoto, Japan – sequence: 7 givenname: Megumi surname: Nagao fullname: Nagao, Megumi organization: Graduate School of Global Environmental Studies, Kyoto University, Kyoto, Japan – sequence: 8 givenname: Tomoaki surname: Okuda fullname: Okuda, Tomoaki organization: Faculty of Science and Technology, Keio University, Kanagawa, Japan – sequence: 9 givenname: Yutaka surname: Kawahito fullname: Kawahito, Yutaka organization: Inflammation and Immunology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan – sequence: 10 givenname: Hirohisa surname: Takano fullname: Takano, Hirohisa organization: Graduate School of Global Environmental Studies, Kyoto University, Kyoto, Japan |
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Keywords | Desert sand dust ASD Necroptosis Asian sand dust AM IL-1α Alveolar macrophages PM |
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•The study uses fine Asian sand dust particles, with a high impact on the lungs.•Asian sand dust is rapidly phagocytosed by alveolar... Asian sand dust (ASD), a significant desert sand dust, contains sub-2.5 µm fine particles and adversely affects human health, particularly exacerbating... Asian sand dust (ASD), a significant desert sand dust, contains sub-2.5 µm fine particles and adversely affects human health, particularly exacerbating... |
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StartPage | 109178 |
SubjectTerms | air Air Pollutants - toxicity Alveolar macrophages Animals Asian sand dust Cell Death - drug effects chemokines Desert sand dust Dust endotoxins environment human health humans IL-1α inflammation Interleukin-1alpha lungs macrophages Macrophages, Alveolar - drug effects Male Mice Mice, Inbred C57BL Necroptosis neutrophils phagocytosis Phagocytosis - drug effects Pneumonia - chemically induced Pneumonia - pathology Sand Silicon Dioxide therapeutics |
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Title | Acceleration of acute lung inflammation by IL-1α released through cell death of alveolar macrophages upon phagocytosis of fine Asian sand dust particles |
URI | https://dx.doi.org/10.1016/j.envint.2024.109178 https://www.ncbi.nlm.nih.gov/pubmed/39662280 https://www.proquest.com/docview/3146651515 https://www.proquest.com/docview/3165860696 https://doaj.org/article/1b4ad3b033fc4cfab4cffdedb5671663 |
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