Decreased serum and bronchoalveolar lavage levels of clara cell secretory protein (CC16) is associated with bronchiolitis obliterans syndrome and airway neutrophilia in lung transplant recipients1

2002 ◽  
Vol 73 (8) ◽  
pp. 1264-1269 ◽  
Author(s):  
Magnus Nord ◽  
Katja Schubert ◽  
Tobias N. Cassel ◽  
Olof Andersson ◽  
Gerdt C. Riise
2010 ◽  
Vol 90 (3) ◽  
pp. 340-342 ◽  
Author(s):  
Annelieke W. M. Paantjens ◽  
Henny G. Otten ◽  
Walter G. J. van Ginkel ◽  
Diana A. van Kessel ◽  
Jules M. M. van den Bosch ◽  
...  

2005 ◽  
Vol 98 (4) ◽  
pp. 1264-1271 ◽  
Author(s):  
Sawako Yoshikawa ◽  
Takashige Miyahara ◽  
Susan D. Reynolds ◽  
Barry R. Stripp ◽  
Mircea Anghelescu ◽  
...  

Lung vascular permeability is acutely increased by high-pressure and high-volume ventilation. To determine the roles of mechanically activated cytosolic PLA2 (cPLA2) and Clara cell secretory protein (CCSP), a modulator of cPLA2 activity, we compared lung injury with and without a PLA2 inhibitor in wild-type mice and CCSP-null mice (CCSP−/−) ventilated with high and low peak inflation pressures (PIP) for 2- or 4-h periods. After ventilation with high PIP, we observed significant increases in the bronchoalveolar lavage albumin concentrations, lung wet-to-dry weight ratios, and lung myeloperoxidase in both genotypes compared with unventilated controls and low-PIP ventilated mice. All injury variables except myeloperoxidase were significantly greater in the CCSP−/− mice relative to wild-type mice. Inhibition of cPLA2 in wild-type and CCSP−/− mice ventilated at high PIP for 4 h significantly reduced bronchoalveolar lavage albumin and total protein and lung wet-to-dry weight ratios compared with vehicle-treated mice of the same genotype. Membrane phospho-cPLA2 and cPLA2 activities were significantly elevated in lung homogenates of high-PIP ventilated mice of both genotypes but were significantly higher in the CCSP−/− mice relative to the wild-type mice. Inhibition of cPLA2 significantly attenuated both the phospho-cPLA2 increase and increased cPLA2 activity due to high-PIP ventilation. We propose that mechanical activation of the cPLA2 pathway contributes to acute high PIP-induced lung injury and that CCSP may reduce this injury through inhibition of the cPLA2 pathway and reduction of proinflammatory products produced by this pathway.


2021 ◽  
pp. 000313482199868
Author(s):  
Fernando A. M. Herbella ◽  
Marco G. Patti

Idiopathic pulmonary fibrosis (IPF) and gastroesophageal reflux disease (GERD) are undoubtedly related. Even though it is not clear yet which one is the primary disease, they certainly interact increasing each other’s severity. Symptoms are unreliable to diagnose GERD in patients with IPF, and objective evaluation with pH monitoring and/or bronchoalveolar lavage analysis is mandatory. Pharmacological treatment with proton pump inhibitors (PPIs) may bring control of IPF in few patients, but PPIs do not control reflux but just change the pH of the gastric refluxate. Surgical therapy based on a fundoplication is safe and effective as it controls any type of reflux, independently from the pH of the gastric refluxate. In patients waiting for lung transplantation (if they can tolerate a laparoscopic operation under general anesthesia), a fundoplication before the operation might block the progression of IPF, while after transplantation it might prevent rejection by preventing the bronchiolitis obliterans syndrome.


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