Ultrastructural changes of the air–blood barrier in mice after intratracheal instillation of lipopolysaccharide and ultrafine carbon black particles

Inoue, Hiromi; Shimada, Akinori; Kaewamatawong, Theerayuth; Naota, Misaki; Morita, Takehito; Ohta, Yasuhiko; Inoue, Ken‐ichiro; Takano, Hirohisa

doi:10.1016/j.etp.2007.10.001

Cited by 17 publications

(15 citation statements)

References 22 publications

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“… 28 – 30 PM-induced AM apoptosis 31 leads to further inflammation and compromised host resistance, via abruption and fragmentation of alveolar epithelial cells, denuded basement membrane, and increased number of pinocytic vesicles in close proximity with carbon black, demonstrating that PM locally affects barrier defenses. 32 …”

Section: Resultsmentioning

confidence: 99%

A Systematic Review of Innate Immunomodulatory Effects of Household Air Pollution Secondary to the Burning of Biomass Fuels

Lee

Kinney

Chillrud

et al. 2015

Annals of Global Health

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BACKGROUND Household air pollution (HAP)-associated acute lower respiratory infections cause 455,000 deaths and a loss of 39.1 million disability-adjusted life years annually. The immunomodulatory mechanisms of HAP are poorly understood. OBJECTIVES The aim of this study was to conduct a systematic review of all studies examining the mechanisms underlying the relationship between HAP secondary to solid fuel exposure and acute lower respiratory tract infection to evaluate current available evidence, identify gaps in knowledge, and propose future research priorities. METHODS We conducted and report on studies in accordance with the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines. In all, 133 articles were fully reviewed and main characteristics were detailed, namely study design and outcome, including in vivo versus in vitro and pollutants analyzed. Thirty-six studies were included in a nonexhaustive review of the innate immune system effects of ambient air pollution, traffic-related air pollution, or wood smoke exposure of developed country origin. Seventeen studies investigated the effects of HAP-associated solid fuel (biomass or coal smoke) exposure on airway inflammation and innate immune system function. RESULTS Particulate matter may modulate the innate immune system and increase susceptibility to infection through a) alveolar macrophage-driven inflammation, recruitment of neutrophils, and disruption of barrier defenses; b) alterations in alveolar macrophage phagocytosis and intracellular killing; and c) increased susceptibility to infection via upregulation of receptors involved in pathogen invasion. CONCLUSIONS HAP secondary to the burning of biomass fuels alters innate immunity, predisposing children to acute lower respiratory tract infections. Data from biomass exposure in developing countries are scarce. Further study is needed to define the inflammatory response, alterations in phagocytic function, and upregulation of receptors important in bacterial and viral binding. These studies have important public health implications and may lead to the design of interventions to improve the health of billions of people daily.

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Section: Resultsmentioning

confidence: 99%

A Systematic Review of Innate Immunomodulatory Effects of Household Air Pollution Secondary to the Burning of Biomass Fuels

Lee

Kinney

Chillrud

et al. 2015

Annals of Global Health

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“…As to the mechanisms of damages of the alveolar wall by LPS, it is suggested that macrophages and neutrophils activated by LPS release free radicals resulting in the degeneration of the air-blood barrier. Translocation of NPs from the air-blood barrier to the capillary lumen may take place through the degenerated structures with acute inflammatory condition [15, 17]. …”

Section: Discussionmentioning

confidence: 99%

“…Preexisting respiratory disorders (e.g., inflammation) may modify the effects of NPs on the respiratory tract and can influence the amount of translocated material. Under normal conditions, lungs are often primed with endotoxins from the inhaled air [15]. We hypothesized that preexisting inflammation may influence the ability of Au NPs to pass through the pulmonary barrier and other organs in the body.…”

Section: Introductionmentioning

confidence: 99%

Prior Lung Inflammation Impacts on Body Distribution of Gold Nanoparticles

Hussain

Vanoirbeek

Haenen

et al. 2013

BioMed Research International

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Introduction. Gold- (Au-) based nanomaterials have shown promising potential in nanomedicine. The individual health status is an important determinant of the response to injury/exposure. It is, therefore, critical to evaluate exposure to Au-nanomaterials with varied preexisting health status. Objective. The goal of this research was to determine the extent of extrapulmonary translocation from healthy and inflamed lungs after pulmonary exposure to AuNPs. Male BALB/c mice received a single dose of 0.8 mg · kg−1 AuNPs (40 nm) by oropharyngeal aspiration 24 hours after priming with LPS (0.4 mg · kg−1) through the same route. Metal contents were analyzed in different organs by inductively coupled plasma-mass spectrometry (ICP-MS). Results. Oropharyngeal aspiration resulted in high metal concentrations in lungs (P < 0.001); however, these were much lower after pretreatment with LPS (P < 0.05). Significantly higher concentrations of Au were detected in heart and thymus of healthy animals, whereas higher concentrations of Au NPs were observed in spleen in LPS-primed animals. Conclusions. The distribution of AuNPs from lungs to secondary target organs depends upon the health status, indicating that targeting of distinct secondary organs in nanomedicine needs to be considered carefully under health and inflammatory conditions.

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“…Additionally, there is experimental evidence that respiratory exposure to nanoparticles may promote thrombosis [10,11]. It has been suggested that lung injury increases the degree of the nanoparticle translocation [12]. For a better understanding of the potential hazards of inhaled nanoparticles it is important to establish whether nanoparticles are translocated, i.e.…”

Section: Introductionmentioning

confidence: 99%

Biodistribution of gold nanoparticles in mouse lung following intratracheal instillation

Sadauskas

Jacobsen

Danscher

et al. 2009

Chemistry Central Journal

140

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BackgroundThe fate of gold nanoparticles, 2, 40 and 100 nm, administered intratracheally to adult female mice was examined. The nanoparticles were traced by autometallography (AMG) at both ultrastructural and light microscopic levels. Also, the gold content was quantified by inductively coupled plasma mass spectrometry (ICP-MS) and neutron activation analysis (NAA). The liver is the major site of deposition of circulating gold nanoparticles. Therefore the degree of translocation was determined by the hepatic deposition of gold. Mice were instilled with 5 intratracheal doses of gold nanoparticles distributed over a period of 3 weeks and were killed 24 h after the last dose. One group of mice were given a single intratracheal dose and were killed after 1 h.ResultsThe instilled nanoparticles were found in lung macrophages already 1 h after a single instillation. In mice instilled treated repeatedly during 3 weeks, the load was substantial. Ultrastructurally, AMG silver enhanced gold nanoparticles were found in lysosome-/endosome-like organelles of the macrophages and analysis with AMG, ICP-MS and NAA of the liver revealed an almost total lack of translocation of nanoparticles. In mice given repeated instillations of 2 nm gold nanoparticles, 1.4‰ (by ICP-MS) to 1.9‰ (by NAA) of the instilled gold was detected in the liver. With the 40 nm gold, no gold was detected in the liver (detection level 2 ng, 0.1‰) except for one mouse in which 3‰ of the instilled gold was found in the liver. No gold was detected in any liver of mice instilled with 100 nm gold (detection level 2 ng, 0.1‰) except in a single animal with 0.39‰ of the dose in the liver.ConclusionWe found that that: (1) inert gold nanoparticles, administered intratracheally are phagocytosed by lung macrophages; (2) only a tiny fraction of the gold particles is translocated into systemic circulation. (3) The translocation rate was greatest with the 2 nm gold particles.

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Ultrastructural changes of the air–blood barrier in mice after intratracheal instillation of lipopolysaccharide and ultrafine carbon black particles

Cited by 17 publications

References 22 publications

A Systematic Review of Innate Immunomodulatory Effects of Household Air Pollution Secondary to the Burning of Biomass Fuels

A Systematic Review of Innate Immunomodulatory Effects of Household Air Pollution Secondary to the Burning of Biomass Fuels

Prior Lung Inflammation Impacts on Body Distribution of Gold Nanoparticles

Biodistribution of gold nanoparticles in mouse lung following intratracheal instillation

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