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 inEnvironment international Vol. 194; p. 109178
Main Authors Sagawa, Tomoya, Ichinose, Takamichi, Honda, Akiko, Kuroda, Etsushi, Ishikawa, Raga, Miyasaka, Natsuko, Nagao, Megumi, Okuda, Tomoaki, Kawahito, Yutaka, Takano, Hirohisa
Format Journal Article
LanguageEnglish
Published Netherlands Elsevier Ltd 01.12.2024
Elsevier
Subjects
Online AccessGet full text
ISSN0160-4120
1873-6750
1873-6750
DOI10.1016/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.
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
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  organization: Inflammation and Immunology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan
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  givenname: Hirohisa
  surname: Takano
  fullname: Takano, Hirohisa
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Keywords Desert sand dust
ASD
Necroptosis
Asian sand dust
AM
IL-1α
Alveolar macrophages
PM
Language English
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Snippet [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...
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
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