Circulating Levels of Clara Cell Protein 16 But Not Surfactant Protein D Identify and Quantify Lung Damage in Patients With Multiple Injuries

2011 ◽  
Vol 71 (2) ◽  
pp. E31-E36 ◽  
Author(s):  
Sebastian Wutzler ◽  
Thomas Lehnert ◽  
Helmut Laurer ◽  
Mark Lehnert ◽  
Marco Becker ◽  
...  
Keyword(s):  
Surfactant Protein ◽  
Lung Damage ◽  
Clara Cell ◽  
Multiple Injuries ◽  
Cell Protein ◽  
Surfactant Protein D ◽  
Clara Cell Protein ◽  
Circulating Levels

scholarly journals Protective effect of extracorporeal membrane pulmonary oxygenation combined with cardiopulmonary resuscitation on post-resuscitation lung injury: a randomised controlled trial

2020 ◽  
Author(s):  
Jiyang Ling ◽  
Chunsheng Li ◽  
Yun Zhang ◽  
Xiaoli Yuan ◽  
Bo Liu ◽  
...  
Keyword(s):  
Superoxide Dismutase ◽  
Protein A ◽  
Surfactant Protein ◽  
Spontaneous Circulation ◽  
Clara Cell ◽  
Surfactant Protein A ◽  
Cell Protein ◽  
Surfactant Protein D ◽  
Lung Water ◽  
Pulmonary Vascular Permeability

Abstract Background: This work examines the protective effect and mechanisms of early extracorporeal membrane oxygenation with cardiopulmonary resuscitation (CPR) on ventricular-fibrillation-induced post-resuscitation lung injury in a swine cardiac-arrest model. Methods: Sixteen male swine were randomised to conventional CPR (CCPR; n=8; CCPR alone) and extracorporeal CPR (ECPR; n=8; extracorporeal membrane oxygenation with CCPR), with restoration of spontaneous circulation for 6 h as an endpoint. Serological specimens were collected at baseline and restoration of spontaneous circulation for 1, 2, 4, and 6 h; lung tissue specimens were obtained postmortem. Between-group comparisons of recovery success rate, extravascular lung water , pulmonary vascular permeability index, electron microscopic features, and serum and tissue biomarkers (surfactant protein A, surfactant protein D, Clara cell protein 16, superoxide dismutase, malondialdehyde, myeloperoxidase) were undertaken. Results: The CCPR group had non-significantly lower 6-h survival rate ( p> 0.05). Serum levels of surfactant protein A, surfactant protein D, Clara cell protein 16, and malondialdehyde were significantly higher ( p< 0.05), whereas serum superoxide dismutase was significantly lower, in the CCPR than in the ECPR group ( p <0.01). Compared with the ECPR group, tissue surfactant protein A, surfactant protein D, and superoxide dismutase significantly decreased compared to the baseline, whereas malondialdehyde and myeloperoxidase significantly increased ( p< 0.01) in the CCPR group. Extravascular lung water and pulmonary vascular permeability index were significantly higher in the CCPR after 6 h compared to the baseline values and the ECPR group ( p< 0.01). Conclusions: Electron microscopy revealed mostly vacuolated intracellular alveolar type II lamellar bodies and fuzzy lamellar structure and widening and blurring of the blood–gas barrier in the CCPR group in contrast to that in the ECPR group. ECPR was found to have protective pulmonary effects, possibly related to the regulation of alveolar surface-active proteins and mitigated oxidative stress response post-resuscitation.

scholarly journals O3C.5 Reduced serum clara cell protein (CC16) as an early pulmonary injury marker for fine particulate matter exposure in occupational population

2019 ◽  
Vol 76 (Suppl 1) ◽  
pp. A26.3-A27
Author(s):  
Huawei Duan ◽  
Yanhua Wang ◽  
Zhenjie Wang ◽  
Ting Wang
Keyword(s):  
Particulate Matter ◽  
Lung Function ◽  
Fine Particulate Matter ◽  
Surfactant Protein ◽  
Exposed Group ◽  
Clara Cell ◽  
Cell Protein ◽  
Pulmonary Injury ◽  
Clara Cell Protein ◽  
Fine Particulate

BackgroundParticulate matter is the key component of air pollutants, mainly produced by emissions of coal-fired plants and road traffic. Exposure to fine particulate matter (PM2.5) pollution is associated with increased morbidity and mortality for respiratory diseases. However, few population-based studies have been conducted to assess the alterations of circulating pulmonary proteins due to long-term PM2.5 exposure.MethodsWe designed a two-stage study. At the first stage, we enrolled 558 coke plant workers with a wide range of PM2.5 exposure levels as the exposed group and 210 controls in China. Pulmonary injury was measured by lung function and serum Clara cell protein (CC16), surfactant protein A (SP-A), and surfactant protein D (SP-D). Linear regression models were used to assess the associations between PM2.5, pulmonary injury markers, and lung function. At the second stage, significant initial findings were validated by an independent diesel engine exhaust (DEE) cohort with 50 DEE exposed workers and 50 controls.ResultsSerum CC16 decreased in a dose-response manner in association with both external and internal PM2.5 exposures in two cohorts. In the first stage, serum CC16 levels decreased with increasing duration of occupational PM2.5 exposure history. An IQR (122.0 μg/m3) increase in PM2.5 was associated with a 5.76% decrease in serum CC16, whereas an IQR (1.06 μmol/mol creatinine) increase in urinary 1-OHP concentration was associated with a 5.36% decrease in serum CC16 in the COE cohort. In the validation stage, the concentration of serum CC16 in PM2.5 exposed group were 22.42% lower than that of the control and an IQR (1.24 μmol/mol creatinine) increase in urinary 1-OHP concentration was associated with a 12.24% decrease in serum CC16 in DEE cohort.ConclusionsReduction of serum CC16 may be a sensitive marker for pulmonary damage in populations with high PM2.5 exposure.

Infant frequent wheezing correlated to Clara cell protein 10 (CC10) polymorphism and concentration, but not allergy sensitization, in a perinatal cohort study

2007 ◽  
Vol 120 (4) ◽  
pp. 842-848 ◽  
Author(s):  
Kuender D. Yang ◽  
Chia-Yu Ou ◽  
Jen-Chieh Chang ◽  
Rong-Fu Chen ◽  
Chieh-An Liu ◽  
...  
Keyword(s):  
Cohort Study ◽  
Clara Cell ◽  
Cell Protein ◽  
Clara Cell Protein

Clara Cell Protein–positive Epithelial Cells Are Reduced in Small Airways of Asthmatics

1999 ◽  
Vol 160 (3) ◽  
pp. 930-933 ◽  
Author(s):  
NORIHARU SHIJUBO ◽  
YOSHIHISA ITOH ◽  
TETSUJI YAMAGUCHI ◽  
AKIHIRO IMADA ◽  
MICHIO HIRASAWA ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Clara Cell ◽  
Cell Protein ◽  
Small Airways ◽  
Clara Cell Protein

scholarly journals Emphysema and extrapulmonary tissue loss in COPD: a multi-organ loss of tissue phenotype

2018 ◽  
Vol 51 (2) ◽  
pp. 1702146 ◽  
Author(s):  
Bartolome R. Celli ◽  
Nicholas Locantore ◽  
Ruth Tal-Singer ◽  
John Riley ◽  
Bruce Miller ◽  
...  
Keyword(s):  
Surfactant Protein ◽  
Forced Expiratory Volume ◽  
Fat Free Mass ◽  
Tissue Loss ◽  
Cell Protein ◽  
Surfactant Protein D ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Club Cell ◽  
Body Compartments

We tested whether emphysema progression accompanies enhanced tissue loss in other body compartments in 1817 patients from the ECLIPSE chronic obstructive pulmonary disease (COPD) cohort.Clinical and selected systemic biomarker measurements were compared in subjects grouped by quantitative tomography scan emphysema quartiles using the percentage of low attenuation area (LAA%). Lowest and highest quartile patients had amino-acid metabolomic profiles. We related LAA% to 3 years decline in lung function (forced expiratory volume in 1 s (FEV1)), body mass index (BMI), fat-free mass index (FFMI) and exacerbations, hospitalisations and mortality rates.Participants with more baseline emphysema had lower FEV1, BMI and FFMI, worse functional capacity, and less cardiovascular disease but more osteoporosis. Systemic C-reactive protein and interleukin-6 levels were similar among groups, but club cell protein 16 was higher and interleukin-8, surfactant protein D and soluble receptor for advanced glycation end product were lower with more emphysema. Metabolomics differed between extreme emphysema quartiles. Patients with more emphysema had accelerated FEV1, BMI and FFMI decline and more exacerbations, hospitalisations and mortality.COPD patients with more emphysema undergo excessive loss of pulmonary and extrapulmonary tissue, which is probably related to abnormal tissue maintenance. Because of worse clinical outcomes, we propose this subgroup be named the multi-organ loss of tissue (MOLT) COPD phenotype.

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