scholarly journals Mucus secretion by single tracheal submucosal glands from normal and cystic fibrosis transmembrane conductance regulator knockout mice

2007 ◽  
Vol 580 (1) ◽  
pp. 301-314 ◽  
Author(s):  
Juan P. Ianowski ◽  
Jae Young Choi ◽  
Jeffrey J. Wine ◽  
John W. Hanrahan
Keyword(s):  
Cystic Fibrosis ◽  
Knockout Mice ◽  
Mucus Secretion ◽  
Transmembrane Conductance Regulator ◽  
Transmembrane Conductance ◽  
Submucosal Glands ◽  
Cystic Fibrosis Transmembrane

CFTR involvement in chloride, bicarbonate, and liquid secretion by airway submucosal glands

1999 ◽  
Vol 277 (4) ◽  
pp. L694-L699 ◽  
Author(s):  
Stephen T. Ballard ◽  
Laura Trout ◽  
Zsuzsa Bebök ◽  
E. J. Sorscher ◽  
Angela Crews
Keyword(s):  
Cystic Fibrosis ◽  
Channel Blocker ◽  
Polyclonal Antibodies ◽  
Surface Epithelium ◽  
Transmembrane Conductance Regulator ◽  
Submucosal Gland ◽  
Transmembrane Conductance ◽  
Active Secretion ◽  
Submucosal Glands ◽  
Cystic Fibrosis Transmembrane

Previous studies demonstrated that ACh-induced liquid secretion by porcine bronchi is driven by active Cl− and H[Formula: see text] secretion. The present study was undertaken to determine whether this process was localized to submucosal glands and mediated by the cystic fibrosis transmembrane conductance regulator (CFTR). When excised, cannulated, and treated with ACh, porcine bronchi secreted 15.6 ± 0.6 μl ⋅ cm−2 ⋅ h−1. Removal of the surface epithelium did not significantly affect the rate of secretion, indicating that the source of the liquid was the submucosal glands. Pretreatment with diphenylamine-2-carboxylate, a relatively nonselective Cl−-channel blocker, significantly reduced liquid secretion by 86%, whereas pretreatment with DIDS, which inhibits a variety of Cl− channels but not CFTR, had no effect. When bronchi were pretreated with glibenclamide or 5-nitro-2-(3-phenylpropylamino)benzoic acid (both inhibitors of CFTR), the rate of ACh-induced liquid secretion was significantly reduced by 39 and 91%, respectively, compared with controls. Agents that blocked liquid secretion also caused disproportionate reductions in H[Formula: see text] secretion. Polyclonal antibodies to the CFTR bound preferentially to submucosal gland ducts and the surface epithelium, suggesting that this channel was localized to these sites. These data suggest that ACh-induced gland liquid secretion by porcine bronchi is driven by active secretion of both Cl− and H[Formula: see text] and is mediated by the CFTR.

scholarly journals Cystic fibrosis transmembrane conductance regulator knockout mice exhibit aberrant gastrointestinal microbiota

Gut Microbes ◽  
2013 ◽  
Vol 4 (1) ◽  
pp. 41-47 ◽  
Author(s):  
Susan V. Lynch ◽  
Katherine C. Goldfarb ◽  
Yvette K. Wild ◽  
Weidong Kong ◽  
Robert C. De Lisle ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Knockout Mice ◽  
Transmembrane Conductance Regulator ◽  
Gastrointestinal Microbiota ◽  
Transmembrane Conductance ◽  
Cystic Fibrosis Transmembrane

scholarly journals Pseudomonas aeruginosa Alginate Promotes Burkholderia cenocepacia Persistence in Cystic Fibrosis Transmembrane Conductance Regulator Knockout Mice

2010 ◽  
Vol 78 (3) ◽  
pp. 984-993 ◽  
Author(s):  
Sangbrita S. Chattoraj ◽  
Rachana Murthy ◽  
Shyamala Ganesan ◽  
Joanna B. Goldberg ◽  
Ying Zhao ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Pseudomonas Aeruginosa ◽  
Knockout Mice ◽  
Bacterial Load ◽  
Burkholderia Cenocepacia ◽  
Respiratory Pathogen ◽  
Transmembrane Conductance Regulator ◽  
Transmembrane Conductance ◽  
Innate Defense ◽  
Cystic Fibrosis Transmembrane

ABSTRACT Pseudomonas aeruginosa, a major respiratory pathogen in cystic fibrosis (CF) patients, facilitates infection by other opportunistic pathogens. Burkholderia cenocepacia, which normally infects adolescent patients, encounters alginate elaborated by mucoid P. aeruginosa. To determine whether P. aeruginosa alginate facilitates B. cenocepacia infection in mice, cystic fibrosis transmembrane conductance regulator knockout mice were infected with B. cenocepacia strain BC7 suspended in either phosphate-buffered saline (BC7/PBS) or P. aeruginosa alginate (BC7/alginate), and the pulmonary bacterial load and inflammation were monitored. Mice infected with BC7/PBS cleared all of the bacteria within 3 days, and inflammation was resolved by day 5. In contrast, mice infected with BC7/alginate showed persistence of bacteria and increased cytokine levels for up to 7 days. Histological examination of the lungs indicated that there was moderate to severe inflammation and pneumonic consolidation in isolated areas at 5 and 7 days postinfection in the BC7/alginate group. Further, alginate decreased phagocytosis of B. cenocepacia by professional phagocytes both in vivo and in vitro. P. aeruginosa alginate also reduced the proinflammatory responses of CF airway epithelial cells and alveolar macrophages to B. cenocepacia infection. The observed effects are specific to P. aeruginosa alginate, because enzymatically degraded alginate or other polyuronic acids did not facilitate bacterial persistence. These observations suggest that P. aeruginosa alginate may facilitate B. cenocepacia infection by interfering with host innate defense mechanisms.

Sign in / Sign up

Export Citation Format

Share Document