scholarly journals Clara Cell Protein Expression in Human Neonates During Respiratory Distress Syndrome

2012 ◽  
Vol 29 (5-6) ◽  
pp. 753-760 ◽  
Author(s):  
Joel Arias-Martínez ◽  
Miguel Palacios-Sánchez ◽  
Dagoberto Delgado-Franco ◽  
José Guzmán-Bárcenas ◽  
Ethel García-Latorre ◽  
...  
2006 ◽  
Vol 32 (8) ◽  
pp. 1167-1174 ◽  
Author(s):  
Olivier Lesur ◽  
◽  
Stephan Langevin ◽  
Yves Berthiaume ◽  
Martin Légaré ◽  
...  

2017 ◽  
Vol 2017 ◽  
pp. 1-5 ◽  
Author(s):  
José Guzmán-Bárcenas ◽  
Antonio Calderón-Moore ◽  
Héctor Baptista-González ◽  
Claudine Irles

The aim of this pilot study was to determine Clara cell protein (CC16) concentration in bronchoalveolar lavages (BAL) fluid from full-term and preterm (<37 weeks’ gestational age) neonates requiring respiratory support, having symptoms of neonatal respiratory distress syndrome, and at risk of bronchopulmonary dysplasia (BPD). We hypothesized that CC16 may be predictive of BPD diagnosis regardless of gestational age. BAL fluid CC16 was measured by ELISA at birth and at day 7 of life. Both groups that developed BPD showed significantly decreased BAL fluid CC16 levels compared to those infants that did not develop the disease. CC16 positively correlated with diagnosis of BPD and negatively with the severity of the disease. These results suggest that BAL fluid CC16 levels may have a diagnostic value at day 7 for BPD in both term and preterm infants. This study demonstrates the potential utility of BAL fluid CC16 levels as a biomarker for BPD in term infants.


Shock ◽  
2020 ◽  
Vol 53 (3) ◽  
pp. 317-326 ◽  
Author(s):  
Ernesto Lopez ◽  
Osamu Fujiwara ◽  
Christina Nelson ◽  
Melissa E. Winn ◽  
Richard S. Clayton ◽  
...  

2013 ◽  
Vol 32 (2) ◽  
pp. 146-151
Author(s):  
Xiaojuan Yin ◽  
Yan Wang ◽  
Lu Xie ◽  
Xiangyong Kong ◽  
Chunzhi Wang ◽  
...  

Summary Background: The aim of this study was to investigate the role of pulmonary surfactant-associated protein B (SP-B) expression in the pathogenesis of neonatal respiratory distress syndrome (RDS) via detecting the protein and mRNA expression of SP-B. Methods: A total of 60 unrelated neonates who died of RDS were chosen as the RDS group and then subgrouped into ≤32 weeks group, 32∼37 weeks group and ≥37 weeks group (n=20). Sixty neonates who died of other diseases were enrolled as controls and subdivided into 3 matched groups based on the gestational age. Western blot assay and RT-PCR were employed. Results: In the RDS group, SP-B protein expression was reduced or deficient in 8 neonates of which 6 had no SP-B protein expression. In the control group, only 1 had reduced SP-B protein expression. The reduced or deficient SP-B protein expression in 9 neonates of both groups was noted in the ≥37 weeks group. In the RDS group, the SP-B mRNA expression was significantly lower than that in the control group. In the ≤37 weeks group, SP-B mRNA expression was comparable between the RDS group and control group. In the 32∼37 weeks group, the SP-B mRNA expression in the RDS group was significantly reduced when compared with the control group. In the ≥37 weeks group, the SP-B mRNA expression in the RDS group was dramatically lower than that in the control group. Conclusions: Alteration of SP-B expression is present at transcriptional and translational levels. Reduction of SP-B mRNA and protein expression is involved in the pathogenesis of RDS.


2007 ◽  
Vol 292 (6) ◽  
pp. L1345-L1351 ◽  
Author(s):  
Theresa R. Grover ◽  
Tiina M. Asikainen ◽  
John P. Kinsella ◽  
Steven H. Abman ◽  
Carl W. White

Respiratory distress syndrome (RDS) secondary to preterm birth and surfactant deficiency is characterized by severe hypoxemia, lung injury, and impaired production of nitric oxide (NO) and vascular endothelial growth factor (VEGF). Since hypoxia-inducible factors (HIFs) mediate the effects of both NO and VEGF in part through regulation by prolyl-hydroxylase-containing domains (PHDs) in the presence of oxygen, we hypothesized that HIF-1α and -2α in the lung are decreased following severe RDS in preterm neonatal lambs. To test this hypothesis, fetal lambs were delivered at preterm gestation (115-day gestation, term = 145 days; n = 4) and mechanically ventilated for 4 h. Lambs developed respiratory failure characterized by severe hypoxemia despite treatment with mechanical ventilation with high inspired oxygen concentrations. Lung samples were compared with nonventilated control animals at preterm (115-day gestation; n = 3) and term gestation (142-day gestation; n = 3). We found that HIF-1α protein expression decreased ( P < 0.05) and PHD-2 expression increased ( P < 0.005) at birth in normal term animals before air breathing. Compared with age-matched controls, HIF-1α protein and HIF-2α protein expression decreased by 80% and 55%, respectively ( P < 0.005 for each) in preterm lambs with RDS. Furthermore, VEGF mRNA was decreased by 40%, and PHD-2 protein expression doubled in RDS lambs. We conclude that pulmonary expression of HIF-1α, HIF-2α, and the downstream target of their regulation, VEGF mRNA, is impaired following RDS in neonatal lambs. We speculate that early disruption of HIF and VEGF expression after preterm birth and RDS may contribute to long-term abnormalities in lung growth, leading to bronchopulmonary dysplasia.


2001 ◽  
Vol 95 (4) ◽  
pp. 974-982 ◽  
Author(s):  
Yoram G. Weiss ◽  
John Tazelaar ◽  
Beth A. Gehan ◽  
Arthur Bouwman ◽  
Melpo Christofidou-Solomidou ◽  
...  

Background Adenoviral-targeted gene delivery to respiratory epithelium can augment production of specific proteins. Therefore, it may be valuable in treating the acute respiratory distress syndrome. The authors tested the hypothesis that adenoviral vector uptake after cecal ligation and double puncture in rats, an animal model of the acute respiratory distress syndrome, is higher than that observed in controls that did not undergo operation ("nonoperated") or those that underwent a sham operation ("sham-operated"). Methods Adenoviruses expressing green fluorescent protein or Lac-Z were delivered into the lungs of anesthetized rats via tracheal catheter. Animals were killed 24 or 48 h later. Histopathology and green fluorescent protein expression were examined using light of fluorescence microscopy. Cellular localization of Lac-Z was determined with electron microscopy or semithin sectioning. Viral receptor density and localization were determined using imunoblotting and immunohistochemistry. Results After cecal ligation and double puncture, rats were hypoxic and tachypneic. Alveoli were segmentally consolidated, contained proteinaceous debris and neutrophils, and had thickened septa. Administration of adenoviruses to rats that were sham-operated or underwent cecal ligation and double puncture resulted in high levels of marker protein expression in cells lining alveoli. Use of 3 x 10(11) plaque-forming units instead of 3 x 10(12) plaque-forming units resulted in similar levels of green fluorescent protein expression with negligible viral-mediated lymphocytic infiltration. Semithin section and electron microscopy revealed expression primarily localized to type II alveolar cells. Abundance of alpha(v)beta3 integrins and human coxsackie-adenovirus receptor (receptors that modulate viral attachment and internalization) was increased after cecal ligation and double puncture, predominantly in type II pneumocytes. Conclusions Cecal ligation and double puncture induces histologic and functional changes consistent with the acute respiratory distress syndrome, increases surface expression of viral receptors, and enhances adenoviral-mediated gene transfer.


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