Plasma surfactant D in patients following acute paraquat intoxication

Gil, Hyo‐Wook; Hong, J.; Park, Jae Ho; Seo, Yun-Seok; Yang, Jong‐Oh; Lee, Eun Young; Hong, Sae‐Yong

doi:10.1080/15563650701338138

Cited by 9 publications

(5 citation statements)

References 14 publications

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“…Elevation of systemic levels of SP-D with smoking, COPD, or other lung injuries is believed to reflect ongoing damage associated with disruption of the alveolar epithelial integrity (16,18,37,38). In our cohort, plasma SP-D levels did not correlate with monocyte MMP-9 production ( Figure 5B) (r 5 0.08; P 5 0.52).…”

Section: Monocyte Mmp-9 Levels Do Not Correlate With Systemic Markersmentioning

confidence: 61%

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

Atkinson¹,

Lutey²,

Suzuki³

et al. 2011

Am J Respir Crit Care Med

115

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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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Section: Monocyte Mmp-9 Levels Do Not Correlate With Systemic Markersmentioning

confidence: 61%

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

Atkinson¹,

Lutey²,

Suzuki³

et al. 2011

Am J Respir Crit Care Med

115

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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%

“…SP-D levels have also been proposed to correlate with genetic elements [61][62][63], body mass index (BMI) [64][65][66][67][68], age [65], circadian rhythm [69], and with particle exposure [70,71] and cigarette smoking habits [25,27,28,31,37,[72][73][74][75][76][77]. In addition, there have been studies examining the levels of SP-D in subjects with Turner syndrome [78], paraquat intoxication [79], swimming in variably treated waters [80], lung transplant patients [81], patients undergoing neurosurgical operations [82], drowning victims [83], polymyositis/dermatomyositis [84], dementia [85], lupus [86], and sleep apnea [87].…”

Section: Introductionmentioning

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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“…Also there are some markers for alveolar destruction in acute PQ intoxication, such as ethane in exhaled breath (15), and plasma surfactant levels (16). …”

Section: Introductionmentioning

confidence: 99%

The Area of Ground Glass Opacities of the Lungs as a Predictive Factor in Acute Paraquat Intoxication

et al. 2009

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Even though plasma paraquat (PQ) levels have known to be an informative predictor, many patients succumb at low PQ levels in acute PQ intoxication. This study was designed to see whether the high resolution computerized tomography (HRCT) of the lungs would be a predictive measure in acute PQ intoxication. HRCT of the lungs was obtained from 119 patients with acute PQ intoxication on 7 days after PQ ingestion. The areas with ground glass opacities (GGOs) were evaluated at five levels with the area measurement tool of the picture archiving and communication systems. Among 119 patients, 102 survived and 17 died. The plasma PQ levels were significantly higher in the non-survivors than in the survivors (2.6±4.0 µg/mL vs. 0.2±0.4 µg/mL, P=0.02). The area with GGOs was 2.0±6.4% in the survivors and 73.0± 29.9% in the non-survivors (P<0.001). No patients survived when the area with GGOs was more than 40% but all of the patients survived when the area affected by GGOs was less than 20%. In conclusion, the area of GGOs is a useful predictor of survival in acute PQ intoxication, especially in patients with low plasma PQ levels.

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Plasma surfactant D in patients following acute paraquat intoxication

Cited by 9 publications

References 14 publications

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

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

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

The Area of Ground Glass Opacities of the Lungs as a Predictive Factor in Acute Paraquat Intoxication

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