Pulmonary Macrophages Are Attracted to Inhaled Particles through Complement Activation

Warheit, David B.; Overby, Lila H.; George, Gerwyn; Brody, Arnold R.

doi:10.3109/01902148809062850

Cited by 88 publications

(34 citation statements)

References 20 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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show abstract

“…Carbon black was used in an additional group because it consists also ofultrafine particles yet has a much higher potency than TiO2 to induce in vitro chemotactic serum factors (7). These factors may be potentially important in vivo to facilitate AM particle encounter (8). The dose-response study consisted ofthe groups and intratracheal doses listed in Table 2.…”

Section: Methodsmentioning

confidence: 99%

Role of the alveolar macrophage in lung injury: studies with ultrafine particles

Oberdörster¹,

Ferin²,

Gelein³

et al. 1992

Environ Health Perspect

278

117

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We conducted a series ofexperiments with ultrfine particles (-20 nm) and larger particles (< 200 nm) of "nuisance" dusts to evaluate the involvement of alveolar macrophages (AM) in particle-induced lung injury and particle translocation in rats. After intratracheal instillation of both ultrafine particles and larger particles ofTO2, we found a highly increased interstitial access of the ultrafine particles combined with a large acute infmmatory reaction as determined by lung lavage parameters. An additional experiment revealed that intratracheal nstillation of ph ctized ultrfine 1102 particles (inside AM) prvented both the puhonary inflam ry reaction and the interl access ofthe utrafin particles. Another experiment showed that the influx of polymorphonuclear cells (PMN) into the alveolar space unexpectedly decreased with higher doses ofultrafine particles, wheras alveolar epithelial permeability (protein leakage) increased. The divergence between PMN influx into the alveolar space and changes in alveolar epithelal permeability implies that they are separate events. Pulmonary inflammatory parameters determined by lung lavage analysis correlated best with the surface area ofthe retained particles rather than with their mass, volume, or numbers. Because higher doses resulted in an increased interstitialized fraction of particles, we suggest that inflamatory events induced by particles in the interstitial space can modify the inflammation in the alveolar space detectable by lung lavage. Our results demonstrate the dual role of AM for modifying particle-induced lung injury, i.e., both preventing such injury and contributing to it. We-& conclude that the increased pulmonary toxicity ofultrafine particles is related to their larger surface areaand to their increased interstitial access. Further, we suggest that the inte stizaon ofparticles isimportant for inducion ofpulmonary fibrotic reactions and that ultrafine particles of nuisance dusts should have different threshold limit values for occupational exposure because of their increased puhnonary toxicity.

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“…21 Inhalation studies of normal and emphysematous rats revealed no pulmonary toxicity of MSHA. 17 MSHA also has been used as a negative control particle in a number of in vitro studies, including studies on pulmonary macrophage activation by complement, 22 activation of human bronchial epithelial cells, 23 and induction of the lung myofibroblast PDGF receptor system. 24 These results concur with previous findings that characterize MSHA as benign.…”

Section: Discussionmentioning

confidence: 99%

Does the Harvard/U.S. Environmental Protection Agency Ambient Particle Concentrator Change the Toxic Potential of Particles?

Savage

Lawrence

Katz

et al. 2003

Journal of the Air & Waste Management Association

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Pulmonary Macrophages Are Attracted to Inhaled Particles through Complement Activation

Cited by 88 publications

References 20 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

Role of the alveolar macrophage in lung injury: studies with ultrafine particles

Does the Harvard/U.S. Environmental Protection Agency Ambient Particle Concentrator Change the Toxic Potential of Particles?

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