Reduced alveolar macrophage migration induced by acute ambient particle (PM10) exposure

Barlow, Peter G.; Brown, David M.; Donaldson, Kenneth; MacCallum, J.; Stone, Vicki

doi:10.1007/s10565-007-9033-y

Cited by 31 publications

(15 citation statements)

References 40 publications

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“…44 AMs have previously been shown to migrate toward complement component C5a. 28,45,46 We therefore chose the zymosan-activated FBS (a rich source of C5a) method to measure migratory capacity. We observed that the migratory capacity of AMs did not significantly change at 1 or 5 days after the 24-hour treatment with MWCNT-0.6 μm; however, at 1 and 5 days after treatment with MWCNT-20 μm, AM migratory capacity was markedly decreased.…”

Section: Discussionmentioning

confidence: 99%

Functional consequences for primary human alveolar macrophages following treatment with long, but not short, multiwalled carbon nanotubes

Sweeney¹,

Grandolfo²,

Ruenraroengsak³

et al. 2015

IJN

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Purpose: Multiwalled carbon nanotubes (MWCNTs) are a potential human health hazard, primarily via inhalation. In the lung, alveolar macrophages (AMs) provide the first line of immune cellular defense against inhaled materials. We hypothesized that, 1 and 5 days after treating AMs with short (0.6 μm in length; MWCNT-0.6 μm) and long (20 μm in length; MWCNT-20 μm) MWCNTs for 24 hours, AMs would exhibit increased markers of adverse bioreactivity (cytokine release and reactive oxygen species generation) while also having a modified functional ability (phagocytosis and migration). Methods: Primary human AMs were treated with short and long MWCNTs for 24 hours, 1 and 5 days after which toxicity end points, including cell death, reactive oxygen species generation, and inflammatory mediator release, were measured. AM functional end points involving phagocytic ability and migratory capacity were also measured. Results: AM viability was significantly decreased at 1 and 5 days after treatment with MWCNT-20 μm, while superoxide levels and inflammatory mediator release were significantly increased. At the same time, there was reduced phagocytosis and migratory capacity alongside increased expression of MARCO; this coincided with frustrated phagocytosis observed by scanning electron microscopy. In contrast, the adverse bioreactivity of the shorter MWCNT-0.6 μm with AMs (and any resulting reduction in AM functional ability) was substantially less marked or absent altogether. Conclusion:This study shows that after 24-hour treatment with long, but not short, MWCNTs, AM function is severely affected up to 5 days after the initial exposure. This has potentially significant pathophysiological consequences for individuals who may be intentionally (via therapeutic applications) or unintentionally exposed to these nanomaterials.

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Section: Discussionmentioning

confidence: 99%

Functional consequences for primary human alveolar macrophages following treatment with long, but not short, multiwalled carbon nanotubes

Sweeney¹,

Grandolfo²,

Ruenraroengsak³

et al. 2015

IJN

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“…Barlow and coworkers [54] assessed the effects of intratracheally instilled PM 10 collected from London on macrophage clearance in rats ex vivo . These authors concluded that acute PM 10 exposure has an effect on macrophage phagocytosis and chemotaxis that may be deleterious to particle clearance within the alveolar region of the lung.…”

Section: In Vivo Studiesmentioning

confidence: 99%

Recent Advances in Particulate Matter and Nanoparticle Toxicology: A Review of theIn VivoandIn VitroStudies

Nemmar

Holme

Rosas

et al. 2013

BioMed Research International

234

197

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Epidemiological and clinical studies have linked exposure to particulate matter (PM) to adverse health effects, which may be registered as increased mortality and morbidity from various cardiopulmonary diseases. Despite the evidence relating PM to health effects, the physiological, cellular, and molecular mechanisms causing such effects are still not fully characterized. Two main approaches are used to elucidate the mechanisms of toxicity. One is the use of in vivo experimental models, where various effects of PM on respiratory, cardiovascular, and nervous systems can be evaluated. To more closely examine the molecular and cellular mechanisms behind the different physiological effects, the use of various in vitro models has proven to be valuable. In the present review, we discuss the current advances on the toxicology of particulate matter and nanoparticles based on these techniques.

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“…En las ratas expuestas a ozono + CuSO 4 los macró-fagos presentaron además de vacuolas, pigmento en su citoplasma, lo que implicaría un mayor daño celular. Los macrófagos pigmentados se observan en la bronquiolitis respiratoria o del fumador, en tanto que en la proteinosis alveolar se detectan macrófagos vacuolados y pigmentados 28,29 .…”

Section: Discussionunclassified

Efecto del sulfato de cobre en el daño pulmonar inducido por la exposición crónica intermitente a ozono

et al. 2017

Rev. méd. Chile

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Effect of copper sulphate on the lung damage induced by chronic intermittent exposure to ozone count, proteins, GGT and AP in BALF (p < 0.05). Foamy and pigmented alveolar macrophages were detected in all lungs of these animals (p < 0.001). Conclusions: Intratracheal instillation of a single dose of CuSO 4 in rats previously subjected to a chronic and intermittent exposure to ozone induces a neutrophil pulmonary inflammatory response and cytoplasmic damage in macrophages. (Rev Med Chile 2017; 145: 9-16)

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Reduced alveolar macrophage migration induced by acute ambient particle (PM10) exposure

Cited by 31 publications

References 40 publications

Functional consequences for primary human alveolar macrophages following treatment with long, but not short, multiwalled carbon nanotubes

Functional consequences for primary human alveolar macrophages following treatment with long, but not short, multiwalled carbon nanotubes

Recent Advances in Particulate Matter and Nanoparticle Toxicology: A Review of theIn VivoandIn VitroStudies

Efecto del sulfato de cobre en el daño pulmonar inducido por la exposición crónica intermitente a ozono

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