To create well-differentiated cultures of normal and chronic sinusitis paranasal sinus epithelial cells and to compare their electrophysiologic properties. Design: In vitro investigation using primary sinus epithelial cells, initially cultured on plastic tissue culture dishes. Cells were characterized by means of immunocytochemical analysis and then passaged to air-liquid interface culture conditions. The morphologic features of air-liquid interface cultures were assessed using light and electron microscopy. Epithelial Na ϩ channel, Na ϩ-K ϩ-2Cl − cotransporter, cystic fibrosis transmembrane conductance regulator, and Ca 2ϩ-activated Cl − channel function were investigated in Ussing chambers. Subjects: Specimens were obtained from 15 patients undergoing transsphenoidal pituitary procedures, tumor removal, or trauma repair and from 9 patients with chronic sinusitis. Results: After culture at an air-liquid interface for 21 days, the epithelium was pseudostratified and contained basal, mucous secretory, and ciliated cells. There were no detectable morphologic differences between normal and chronic sinusitis cells. In cultures of normal cells, median basal short circuit current was 4.7 µA/cm 2 , and Na ϩ transport, defined as the amiloride hydrochloridesensitive component, was approximately 20% of the total. Basal and amiloride-sensitive short circuit currents were greater in cultures of chronic sinusitis cells. Basal short circuit currents in both types of cultures were insensitive to the Cl − transport inhibitor bumetanide, but all responded to forskolin or uridine triphosphate. After amiloride pretreatment, forskolin and uridine triphosphate responses were greater in chronic sinusitis cells. Conclusions: We established methods for welldifferentiated sinus epithelial cultures. The cells exhibited Na ϩ absorption and Cl − secretion, and elevated rates of ion transport may be pathophysiologically relevant in chronic sinusitis.
Background: An association between bronchial asthma and sinusitis has long been suspected. Our aim is to study the clinical features of chronic sinusitis associated with bronchial asthma as two manifestations of one airway disease. Methods: We conducted a prospective analysis of the outcome of 88 patients, with or without bronchial asthma, who underwent endoscopic sinus surgery (ESS) for chronic sinusitis. Patients were divided into two groups by the presence or absence of asthma and were evaluated. One surgeon performed the ESS, and the same postoperative treatment was given to both groups. The postoperative outcomes of symptoms and objective findings related to sinusitis were evaluated numerically, with a maximum score of 2 points for each examination item. Twenty-eight patients with asthma symptoms were assessed before and after surgery, using peak flow (liter/second) and medication scores (according to US Food and Drug Administration) to determine whether bronchial asthma was improved by first-time ESS. Results: The outcomes of ESS were signifi- cantly worse in the asthma group, especially the endonasal findings. Patients suffering from chronic sinusitis and bronchial asthma showed improvement following ESS in terms of their asthma symptoms, peak flow and medication score. Patients with a good ESS result tended to have the greatest improvement in their asthma. Conclusions: We conclude that sinusitis and asthma are closely related to each other, acting as two manifestations of one airway disease. We recommend treating cases of sinusitis complicated by asthma as a single disease of the entire respiratory tract.
We investigated regulatory mechanisms of Cl(-) secretion playing an essential role in the maintenance of surface fluid in human airway epithelial Calu-3 cells. The present study reports that quercetin (a flavonoid) stimulated bumetanide-sensitive Cl(-) secretion with reduction of apical Cl(-) conductance, suggesting that quercetin stimulates Cl(-) secretion by activating an entry step of Cl(-) across the basolateral membrane through Na(+)/K(+)/2Cl(-) cotransporter (NKCC1). To clarify the mechanism stimulating NKCC1 by quercetin, we verified involvement of protein kinase (PK)A, PKC, protein tyrosine kinase (PTK), and cytosolic Ca(2+)-dependent pathways. A PKA inhibitor (PKI-14-22 amide), a PKC inhibitor (Gö 6983) or a Ca(2+) chelating agent did not affect the quercetin-stimulated Cl(-) secretion. On the other hand, a PTK inhibitor (AG18) significantly diminished the stimulatory action of quercetin on Cl(-) secretion without inhibitory effects on apical Cl(-) conductance, suggesting that a PTK-mediated pathway is involved in the stimulatory action of quercetin. The quercetin action on Cl(-) secretion was suppressed with brefeldin A (BFA, an inhibitor of vesicular transport from ER to Golgi), and the BFA-sensitive Cl(-) secretion was not observed in the presence of an epidermal growth factor receptor (EGFR) kinase inhibitor (AG1478), suggesting that quercetin stimulates Cl(-) secretion by causing the EGFR kinase-mediated translocation of NKCC1 or an NKC1-activating factor to the basolateral membrane in human airway epithelial Calu-3 cells. However, the surface density of NKCC1 was not increased by quercetin, but quercetin elevated the activity of NKCC1. These observations indicate that quercetin stimulates Cl(-) secretion by activating NKCC1 via translocation of an NKCC1-activating factor through an EGFR kinase-dependent pathway.
JCP sensitization appeared to be associated with the recent birth cohort and to increases in dispersed pollen just after birth and in the observed season. Although the recent birth cohort was more easily sensitized, they were not more likely to develop symptoms. In contrast to JCP sensitization, strong HDM sensitization appeared to develop prior to commencement of primary school and was more likely to affect boys.
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