The objective of this work was to determine if increasing CF transmembrane conductance regulator (CFTR) activity by ivacaftor could treat CF sinus disease and assess its effect on primary sinus epithelial cultures.
Septal PNE exhibit a robust ion transport phenotype and indicate CFTR(-/-) sinus disease could be attributable to diminished alternative pathways for Cl(-) transport.
Using the mnemonic ACHE, this article presents key Anatomy, Clinical cases, How to image, Essential clinical and radiographic features that help the radiologist, otolaryngologist, and neurologist evaluate sinus disease and headaches.
We performed a prospective, controlled trial to detect pulmonary aspiration of radiolabeled albumin applied to the nasal mucosa of study subjects with chronic sinusitis related to CF and control subjects without sinus disease.
By immunohistochemistry and ELISA, samples were studied with respect to urokinase-type plasminogen activator (uPA), uPA receptor (uPAR), plasminogen activator inhibitor-1 (PAI-1) and key mediators in sinus disease, TGF-beta1 and eosinophil cationic protein (ECP).
By immunohistochemistry and ELISA, samples were studied with respect to urokinase-type plasminogen activator (uPA), uPA receptor (uPAR), plasminogen activator inhibitor-1 (PAI-1) and key mediators in sinus disease, TGF-beta1 and eosinophil cationic protein (ECP).
These findings suggest that impaired innate immune responses to pathogens via TLR9 on sinonasal epithelial cells may represent a critical mechanism in chronic inflammatory sinus disease.