Effect of air pollutants on the pulmonary surfactant system

Müller, Volker; Seifart,; Barth,

doi:10.1046/j.1365-2362.1998.00342.x

Cited by 72 publications

(34 citation statements)

References 147 publications

(187 reference statements)

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“…Early studies in animal models indicated a general increase in surfactant volume, but not composition in response to silica [12,13], which according to Muller et al, is unique to silica inhalation compared to tobacco smoke and diesel particles [14]. One study found 3-7 fold increases in PL and SP, respectively, occurring in a rat model with acid-washed silica, but not with unwashed silica [15].…”

Section: Effect Of Silica Exposure On Lung Surfactantmentioning

confidence: 99%

Silica binding and toxicity in alveolar macrophages

Hamilton

Thakur

Holian

2008

Free Radical Biology and Medicine

341

242

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Inhalation of the crystalline form of silica is associated with a variety of pathologies from acute lung inflammation to silicosis, in addition to autoimmune disorders and cancer. Basic science researchers looking at the mechanisms involved with the earliest initiators of disease are focused on how the alveolar macrophage (AM) interacts with the inhaled silica particle and the consequences of silicainduced toxicity on the cellular level. Based on experimental results, several rationales have been developed on exactly how crystalline silica particles are toxic to the macrophage cell that is functionally responsible for clearance of the foreign particle. For example, silica is capable of producing reactive oxygen species (ROS) either directly (on the particle surface) or indirectly (produced by the cell as a response to silica) triggering cell-signaling pathways initiating cytokine release and apoptosis. With murine macrophages, reactive nitrogen species (RNS) are produced in the initial respiratory burst in addition to ROS. An alternative explanation for silica toxicity includes lysosomal permeability, where silica disrupts the normal internalization process leading to cytokine release and cell death. Still other research has focused on the cell surface receptors (collectively known as scavenger receptors) involved in silica binding and internalization. The silica-induced cytokine release and apoptosis is described as the function of receptor-mediated signaling rather than free radical damage. Current research ideas on silica toxicity and binding in the alveolar macrophage are reviewed and discussed.

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Section: Effect Of Silica Exposure On Lung Surfactantmentioning

confidence: 99%

Silica binding and toxicity in alveolar macrophages

Hamilton

Thakur

Holian

2008

Free Radical Biology and Medicine

341

242

View full text Add to dashboard Cite

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“…It is possible that the increased sensitivity to infection that some individuals exhibit after ozone exposure, as assessed by higher risk of common infections in areas with highly polluted air (42), may reflect the involvement of intrinsic or genetic factors and/or the functional impairment of oxidant-exposed SP-A. Different individuals may possess different combinations of SP-A variants and proportions of SP-A1 and SP-A2 content (52).…”

mentioning

confidence: 99%

Impact of ozone exposure on the phagocytic activity of human surfactant protein A (SP-A) and SP-A variants

Mikerov¹,

Umstead²,

Gan³

et al. 2008

American Journal of Physiology-Lung Cellular and Molecular Phys

118

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Surfactant protein A (SP-A) enhances phagocytosis of Pseudomonas aeruginosa. SP-A1 and SP-A2 encode human (h) SP-A; SP-A2 products enhance phagocytosis more than SP-A1. Oxidation can affect SP-A function. We hypothesized that in vivo and in vitro ozone-induced oxidation of SP-A (as assessed by its carbonylation level) negatively affects its function in phagocytosis (as assessed by bacteria cell association). To test this, we used P. aeruginosa, rat alveolar macrophages (AMs), hSP-As with varying levels of in vivo (natural) oxidation, and ozone-exposed SP-A2 (1A, 1A 0 ) and SP-A1 (6A 2 , 6A 4 ) variants. SP-A oxidation levels (carbonylation) were measured; AMs were incubated with bacteria in the presence of SP-A, and the phagocytic index was calculated. We found: 1) the phagocytic activity of hSP-A is reduced with increasing levels of in vivo SP-A carbonylation; 2) in vitro ozone exposure of hSP-A decreases its function in a dose-dependent manner as well as its ability to enhance phagocytosis of either gram-negative or gram-positive bacteria; 3) the activity of both SP-A1 and SP-A2 decreases in response to in vitro ozone exposure of proteins with SP-A2 being affected more than SP-A1. We conclude that both in vivo and in vitro oxidative modifications of SP-A by carbonylation reduce its ability to enhance phagocytosis of bacteria and that the activity of SP-A2 is affected more by in vitro ozone-induced oxidation. We speculate that functional differences between SP-A1 and SP-A2 exist in vivo and that the redox status of the lung microenvironment differentially affects function of SP-A1 and SP-

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“…Air pollutants have also been recognized to influence the structure and function of the lung surfactant system (6,7). Oxidative inactivation of surfactant by cellular reactive oxygen species (ROS), leading to surfactant lipid peroxidation, protein carbonylation, and functional impairment of surfactant protein A, are thought to be possible mechanisms underlying air pollutantinduced surfactant damage (7)(8)(9)(10)(11). Oxidative damage to lung epithelial cells is a component of acute lung injury and associated respiratory failure (12).…”

mentioning

confidence: 99%

Lung Surfactant Gelation Induced by Epithelial Cells Exposed to Air Pollution or Oxidative Stress

Anseth

Goffin

Fuller

et al. 2005

Am J Respir Cell Mol Biol

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Lung surfactant lowers surface tension and adjusts interfacial rheology to facilitate breathing. A novel instrument, the interfacial stress rheometer (ISR), uses an oscillating magnetic needle to measure the shear viscosity and elasticity of a surfactant monolayer at the air-water interface. The ISR reveals that calf lung surfactant, Infasurf, exhibits remarkable fluidity, even when exposed to air pollution residual oil fly ash (ROFA), hydrogen peroxide (H 2 O 2 ), or conditioned media from resting A549 alveolar epithelial cells (AEC). However, when Infasurf is exposed to a subphase of the soluble fraction of ROFA-or H 2 O 2 -treated AEC conditioned media, there is a prominent increase in surfactant elasticity and viscosity, representing twodimensional gelation. Surfactant gelation is decreased when ROFA-AEC are pretreated with inhibitors of cellular reactive oxygen species (ROS), or with a mitochondrial anion channel inhibitor, as well as when A549-0 cells that lack mitochondrial DNA and functional electron transport are investigated. These results implicate both mitochondrial and nonmitochondrial ROS generation in ROFA-AEC-induced surfactant gelation. A549 cells treated with H 2 O 2 demonstrate a dose-dependent increase in lung surfactant gelation. The ISR is a unique and sensitive instrument to characterize surfactant gelation induced by oxidatively stressed AEC.

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Effect of air pollutants on the pulmonary surfactant system

Cited by 72 publications

References 147 publications

Silica binding and toxicity in alveolar macrophages

Silica binding and toxicity in alveolar macrophages

Impact of ozone exposure on the phagocytic activity of human surfactant protein A (SP-A) and SP-A variants

Lung Surfactant Gelation Induced by Epithelial Cells Exposed to Air Pollution or Oxidative Stress

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