Lung epithelium injury biomarkers in workers exposed to sulphur dioxide in a non-ferrous smelter

Haddam, Nahida; Salihović, Samira; Dumont, Xavier; Taleb, Abdesselem; Haufroid, Vincent; Lison, Dominique; Bernard, Alfred

doi:10.1080/13547500902989088

Cited by 11 publications

(8 citation statements)

References 29 publications

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“…These clinical observations are supported by in vitro observations that nicotine can cause reduced levels of SP-D in human airway epithelial cells ( 366 ). Additional studies have demonstrated increased circulating SP-D with tobacco smoking or other types of noxious exposure, including data from a twin study showing that smoking monozygotic twins had markedly increased serum SP-D relative to their non-smoking twins, despite the very high heritability of serum SP-D levels ( 208 , 252 , 280 , 340 , 367 , 368 ); however, smoke-induced serum levels may not be clearly evident in mixed populations of respiratory patients, where SP-D levels may be influenced by other processes ( 369 ). As described earlier, cigarette smoke disrupts the quaternary structure of SP-D molecules ( 252 ).…”

Section: The Role Of Sp-d In Respiratory Diseasementioning

confidence: 99%

Surfactant Protein D in Respiratory and Non-Respiratory Diseases

2018

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Surfactant protein D (SP-D) is a multimeric collectin that is involved in innate immune defense and expressed in pulmonary, as well as non-pulmonary, epithelia. SP-D exerts antimicrobial effects and dampens inflammation through direct microbial interactions and modulation of host cell responses via a series of cellular receptors. However, low protein concentrations, genetic variation, biochemical modification, and proteolytic breakdown can induce decomposition of multimeric SP-D into low-molecular weight forms, which may induce pro-inflammatory SP-D signaling. Multimeric SP-D can decompose into trimeric SP-D, and this process, and total SP-D levels, are partly determined by variation within the SP-D gene, SFTPD. SP-D has been implicated in the development of respiratory diseases including respiratory distress syndrome, bronchopulmonary dysplasia, allergic asthma, and chronic obstructive pulmonary disease. Disease-induced breakdown or modifications of SP-D facilitate its systemic leakage from the lung, and circulatory SP-D is a promising biomarker for lung injury. Moreover, studies in preclinical animal models have demonstrated that local pulmonary treatment with recombinant SP-D is beneficial in these diseases. In recent years, SP-D has been shown to exert antimicrobial and anti-inflammatory effects in various non-pulmonary organs and to have effects on lipid metabolism and pro-inflammatory effects in vessel walls, which enhance the risk of atherosclerosis. A common SFTPD polymorphism is associated with atherosclerosis and diabetes, and SP-D has been associated with metabolic disorders because of its effects in the endothelium and adipocytes and its obesity-dampening properties. This review summarizes and discusses the reported genetic associations of SP-D with disease and the clinical utility of circulating SP-D for respiratory disease prognosis. Moreover, basic research on the mechanistic links between SP-D and respiratory, cardiovascular, and metabolic diseases is summarized. Perspectives on the development of SP-D therapy are addressed.

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Section: The Role Of Sp-d In Respiratory Diseasementioning

confidence: 99%

Surfactant Protein D in Respiratory and Non-Respiratory Diseases

2018

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“…Given that some of the variation seen in the published literature might be explained by the use of different antibodies, we detected SP-D in serum and plasma samples using either the ELISA kit's detection antibody or the polyclonal goat anti-SP-D antibody. While there is no significant difference between detection by the [12,13,[17][18][19]21,25,28,38,[43][44][45]49,50,59,61,77,84,89], BioVendor [14,[31][32][33][34][35][36]46,52,56,64,65,72,75,76,79,80], and Holmskov et al [3,39,[53][54][55]58,62,66,69,70,78,85,86]) were compared. b) The range of healthy control ...…”

Section: Influence Of Detection Antibody On Extrapolated Sp-d Levelmentioning

confidence: 99%

Factors Influencing the Measurement of Plasma/Serum Surfactant Protein D Levels by ELISA

Bratcher

Gaggar

2014

PLoS ONE

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BackgroundExtensive variations in human surfactant protein D (SP-D) levels in circulation as measured by ELISA exist in the published literature. In order to determine the source of these variations, factors influencing the measurement by ELISA were explored.Materials and MethodsPeripheral blood from healthy individuals was collected into various vacutainers during the same blood draw. Recombinant SP-D was diluted into different matrices and used for a standard curve. Samples were analyzed by capture ELISA using one of two distinct detection antibodies.ResultsThe type of matrix had some effects on detection of recombinant SP-D. The type of anticoagulant used and dilution factor had very little effect, except for in plasma collected in EDTA vacutainers. The extent of variation in published values seemed to be due to the ELISA configuration employed, and, in agreement with this, we found that by switching the detection antibody, there was a 50% decrease in the extrapolated SP-D value of serum and plasma samples. Storage of samples resulted in slight changes in measured SP-D levels.ConclusionsThe ELISA configuration employed to measure circulating levels of SP-D has a significant effect on the extrapolated values. In both configurations tested, the use of EDTA as a coagulant resulted in inconsistent values, and we, therefore, suggest the avoidance of this anticoagulant when assaying for SP-D by ELISA. While the demonstrated effects of several factors on measurement of SP-D may not account for all the disparities amongst the previous studies, they stress that variations in methodologies for measuring the same protein can result in very inconsistent results.

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“…Accordingly, we compared circulating monocyte MMP-9 production with the wholelung emphysema severity as determined by quantitative CT scan analysis and with two systemic markers of active lung injury (Clara cell secretory protein [CCSP] and surfactant protein-D [SP-D]) (16)(17)(18) that are altered in current smokers and subjects with COPD (19)(20)(21)(22)(23)(24). Some of the results of this manuscript have been previously published in the form of an abstract (25).…”

Section: What This Study Adds To the Fieldmentioning

confidence: 99%

The Role of Matrix Metalloproteinase-9 in Cigarette Smoke–induced Emphysema

Atkinson¹,

Lutey²,

Suzuki³

et al. 2011

Am J Respir Crit Care Med

114

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Rationale: Matrix metalloprotease (MMP)-9 is an elastolytic endopeptidase produced by activated macrophages that may be involved in the development of human pulmonary emphysema and could be inhibited with existing compounds. Mouse models have demonstrated that excess MMP-9 production can result in permanent alveolar destruction. Objectives: To determine if MMP-9 causes cigarette smoke-induced emphysema using MMP-9 knockout mice and human samples. Methods: Mouse lungs were analyzed for inflammation and airspace enlargement using a mainstream smoke-exposure model. Human macrophage mRNA was isolated from subjects with emphysema by laser capture microdissection. Human blood monocyte mRNA was isolated from subjects with greater than 30 pack-year smoking history. Human gene expression was determined by quantitative polymerase chain reaction and compared with emphysema severity determined by automated computed tomography analysis. Plasma Clara cell secretory protein and surfactant protein-D were quantified to measure ongoing lung injury. Measurements and Main Results: Mice deficient in MMP-9 develop the same degree of cigarette smoke-induced inflammation and airspace enlargement as strain-matched controls. Macrophages are the predominant source of MMP-9 production in human emphysema specimens and similar quantities of macrophage MMP-9 mRNA is present in areas of lung with and without emphysema. Circulating monocytes produce more MMP-9 in individuals with advanced emphysema severity despite no correlation of MMP-9 with markers of ongoing lung damage. Conclusions: These results suggest that MMP-9 in humans who smoke is similar to smoke-exposed mice, where MMP-9 is present in emphysematous lung but not correlated with the emphysema. To the degree that the mechanisms of emphysema in humans who smoke resemble the mouse model, these data suggest specific inhibition of MMP-9 is unlikely to be an effective therapy for cigarette smoke-induced emphysema. Clinical trial registered with www.clinicaltrials.gov (NCT 00757120).Keywords: pulmonary disease, chronic obstructive; laser capture microdissection; mice, knockout Several studies have implicated matrix metalloproteinase-9 (MMP-9, gelatinase B, type IV collagenase B), in emphysema and chronic obstructive pulmonary disease (COPD) pathogenesis (1-5). MMP-9 can be accurately measured and is an elastolytic protease that is produced in large quantities by inflammatory cells, thus making it suitable for investigation in emphysema (5-7). However, because the pathophysiology of emphysema follows such an indolent course, developing over decades in response to cigarette smoke, a link between MMP-9 activity and alveolar destruction is lacking.Mouse models have identified several MMPs that cause airspace enlargement by overexpression (8, 9), or that prevent airspace enlargement by gene deletion in smoking models (10). The recent discovery that mice transgenically altered to overexpress human MMP-9 in alveolar macrophages develop progressive airspace enlargement (8) adds importance to the e...

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Lung epithelium injury biomarkers in workers exposed to sulphur dioxide in a non-ferrous smelter

Cited by 11 publications

References 29 publications

Surfactant Protein D in Respiratory and Non-Respiratory Diseases

Surfactant Protein D in Respiratory and Non-Respiratory Diseases

Factors Influencing the Measurement of Plasma/Serum Surfactant Protein D Levels by ELISA

The Role of Matrix Metalloproteinase-9 in Cigarette Smoke–induced Emphysema

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