scholarly journals Utility of urinary Clara cell protein (CC16) to demonstrate increased lung epithelial permeability in non-smokers exposed to outdoor secondhand smoke

2012 ◽  
Vol 23 (2) ◽  
pp. 183-189 ◽  
Author(s):  
Gideon St Helen ◽  
Nina T Holland ◽  
John R Balmes ◽  
Daniel B Hall ◽  
J Thomas Bernert ◽  
...  
Keyword(s):  
Secondhand Smoke ◽  
Clara Cell ◽  
Cell Protein ◽  
Epithelial Permeability ◽  
Clara Cell Protein ◽  
Lung Epithelial ◽  
Lung Epithelial Permeability

Clara Cell Protein as a Biomarker for Lung Epithelial Injury in Asphalt Workers

2007 ◽  
Vol 49 (10) ◽  
pp. 1073-1078 ◽  
Author(s):  
Bente Ulvestad ◽  
Britt Grethe Randem ◽  
Lena Andersson ◽  
Dag G. Ellingsen ◽  
Lars Barregard
Keyword(s):  
Clara Cell ◽  
Cell Protein ◽  
Epithelial Injury ◽  
Clara Cell Protein ◽  
Lung Epithelial

Lung epithelial injury markers are not influenced by use of lower tidal volumes during elective surgery in patients without preexisting lung injury

2008 ◽  
Vol 294 (2) ◽  
pp. L344-L350 ◽  
Author(s):  
Rogier M. Determann ◽  
Esther K. Wolthuis ◽  
Goda Choi ◽  
Paul Bresser ◽  
Alfred Bernard ◽  
...  
Keyword(s):  
Mechanical Ventilation ◽  
Lung Injury ◽  
Elective Surgery ◽  
Lavage Fluid ◽  
Clara Cell ◽  
Cell Protein ◽  
Epithelial Injury ◽  
Clara Cell Protein ◽  
Lung Epithelial ◽  
Ventilation Strategies

Clara cell protein levels are elevated in plasma of individuals with mild or subclinical lung injury. We studied the influence of two mechanical ventilation strategies on local and systemic levels of Clara cell protein (CC16) and compared them with levels of soluble receptor for advanced glycation end products (sRAGE) and surfactant proteins (SP)-A and -D in patients undergoing elective surgery. Saved samples from a previously reported investigation were used for the study. Forty patients planned for elective surgery were randomized to mechanical ventilation with either a conventional tidal volume (VT) of 12 ml/kg without positive end-expiratory pressure (PEEP) or low VT of 6 ml/kg and 10 cmH2O PEEP. Plasma and bronchoalveolar lavage fluid (BALF) was collected directly after intubation and after 5 h of mechanical ventilation. While systemic levels of SP-A and SP-D remained unchanged, systemic levels of CC16 and sRAGE increased significantly in both groups after 5 h ( P < 0.001 for both). BALF levels of SP-A, SP-D, CC16, and sRAGE remained unaffected. No differences were found between the two mechanical ventilation strategies regarding any of the measured biological markers. In conclusion, systemic levels of CC16 and sRAGE rise after 5 h in patients receiving mechanical ventilation for elective surgery. Mechanical ventilation with lower tidal volumes and PEEP did not have a different effect on levels of biomarkers of lung epithelial injury compared with conventional mechanical ventilation.

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

Asbestos-induced lung epithelial permeability: potential role of nonoxidant pathways

1998 ◽  
Vol 275 (2) ◽  
pp. L262-L268
Author(s):  
Michael W. Peterson ◽  
Jennifer Kirschbaum
Keyword(s):  
Tyrosine Kinase ◽  
Lung Fibrosis ◽  
Human Lung ◽  
Biological Effects ◽  
Tyrosine Phosphatase ◽  
Epithelial Permeability ◽  
Lung Epithelium ◽  
Asbestos Fibers ◽  
Lung Epithelial ◽  
Lung Epithelial Permeability

Asbestos fibers are an important cause of lung fibrosis; however, the biological mechanisms are incompletely understood. The lung epithelium serves an important barrier function in the lung, and disrupting the epithelial barrier can contribute to lung fibrosis. Lung epithelial permeability is increased in patients with asbestosis, and asbestos fibers increase permeability across cultured human lung epithelium. However, the mechanism of this increased permeability is not known. Many of the biological effects of asbestos are postulated to be due to its ability to generate oxidants, and oxidants are known to increase epithelial permeability. However, we previously reported that altering the iron content of asbestos (important in oxidant generation) had no effect on its ability to increase permeability. For that reason, we undertook these studies to determine whether asbestos increases epithelial permeability through nonoxidant pathways. Both extracellular (H2O2) and intracellular (menadione) oxidants increase paracellular permeability across human lung epithelial monolayers. Extracellular catalase but not superoxide dismutase prevented increased permeability after both oxidant exposures. However, catalase offered no protection from asbestos-induced permeability. We next depleted the cells of glutathione or catalase to determine whether depleting normal cellular antioxidants would increase the sensitivity to asbestos. Permeability was the same in control cells and in cells depleted of these antioxidants. In addition to generating oxidants, asbestos also activates signal transduction pathways. Blocking protein kinase C activation did not prevent asbestos-induced permeability; however, blocking tyrosine kinase with tyrophostin A25 did prevent asbestos-induced permeability, and blocking tyrosine phosphatase with sodium vanadate enhanced the effect of asbestos. These data demonstrate that asbestos may increase epithelial permeability through nonoxidant pathways that involve tyrosine kinase activation. This model offers an important system for studying pathways involved in regulating lung epithelial permeability.

Lung epithelial permeability: relation to nonspecific airway responsiveness

1984 ◽  
Vol 57 (1) ◽  
pp. 77-84 ◽  
Author(s):  
P. M. O'Byrne ◽  
M. Dolovich ◽  
R. Dirks ◽  
R. S. Roberts ◽  
M. T. Newhouse
Keyword(s):  
Airway Responsiveness ◽  
Epithelial Permeability ◽  
Lung Epithelial ◽  
Lung Epithelial Permeability

Adipose-derived mesenchymal stem cells ameliorate lung epithelial injury through mitigating of oxidative stress in mustard lung

2020 ◽  
Vol 15 (7) ◽  
pp. 1861-1876
Author(s):  
Eisa Tahmasbpour Marzouni ◽  
Setareh Panahi Dorcheh ◽  
Amir Nejad-Moghaddam ◽  
Mostafa Ghanei ◽  
Hassan Goodarzi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Airway Remodeling ◽  
Pulmonary Function Tests ◽  
Clara Cell ◽  
Cell Protein ◽  
Mucin 1 ◽  
Gradual Improvement ◽  
Potential Efficacy ◽  
Lung Epithelial ◽  
Registration Number

Aim: We investigated potential efficacy of autologous adipose-derived mesenchymal stem cell (MSC) on oxidative stress (OS) and airway remodeling in patients with chronic mustard lung. Patients & methods: Ten patients received 100 × 106 cells every 20 days for 4 injections over a 2-month period. Results: A gradual improvement was observed for 6 min walk test scores, pulmonary function tests and respiratory quality after MSCs therapy. A significant decrease was found for the mean levels of Mucin-1 protein (KL-6; p = 0.022) and Clara cell protein 16 (CC16; p = 0.005). Antioxidants had a tendency to be higher after each injection. Conclusion: Our findings revealed that MSCs therapy can be safely used for improvement of lung injury and regeneration in these patients without adverse effects. Trial registration number: NCT02749448 ( ClinicalTrials.gov )

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