title: Proton secretion in freshly excised sinonasal mucosa from asthma and sinusitis patients.
abstract: BACKGROUND
  Proton (H+) secretion and the HVCN1 H+ channel are part of the innate host defense mechanism of the airways. The objective of this study was to determine H+ secretion in asthmatic and nonasthmatic patients with chronic rhinosinusitis (CRS) in freshly excised human sinonasal tissue.
  
  
  METHODS
  Nasal or sinus mucosa from subjects with three different conditions (normal, CRS, and CRS with asthma) was harvested during sinus surgery. The equilibrium pH and the rate of H+ secretion were measured in an Ussing chamber using the pH-stat titration technique.
  
  
  RESULTS
  Nasal epithelia isolated from subjects with CRS and asthma had a mucosal equilibrium pH = 6.95 (n = 5), which was significantly lower than in normal subjects (7.35 +/- 0.21; n = 5) or from subjects with CRS without asthma (7.33 +/- 0.15 In = 5). Nasal epithelia from CRS with asthma (n = 5) secreted H+ at a rate of 135 +/- 46 nmol x min(-1) x cm(-2). This rate was significantly higher compared with normal (73 +/- 39 nmol x min(-1) x cm(-2); n = 8) or CRS without asthma (51 +/- 28 nmol x min(-1) x cm(-2); n = 7). Mucosal addition of the HVCN1 blocker ZnCl2 blocked H+ secretion by 70% in normal, 53% in CRS without asthma, and by 51% in CRS with asthma. In contrast, measures in sinus tissues were unaffected by the disease condition.
  
  
  CONCLUSIONS
  Freshly excised human nasal and sinus epithelia secrete acid. Nasal (but not sinus) tissues from asthmatic CRS patients showed lower mucosal pH values and higher rates of H+ secretion than CRS and normal subjects. The increased acid secretion might contribute to epithelial injury in CRS patients with asthma.
authors: Division of Rhinology, Department of Otolaryngology-Head and Neck Surgery, Stanford University School of Medicine, Stanford, California, USA.
authors: Do-Yeon
authors: DY
authors: Cho
authors: Mohammad
authors: M
authors: Hajighasemi
authors: Peter H
authors: PH
authors: Hwang
authors: Beate
authors: B
authors: Illek
authors: Horst
authors: H
authors: Fischer
mesh_terms: D001249:Asthma / Q000150:complications / Q000276:immunology / Q000378:metabolism* / Q000503:physiopathology; D002478:Cells, Cultured; D002712:Chlorides / Q000494:pharmacology; D002908:Chronic Disease; D004802:Eosinophilia; D006801:Humans; D006863:Hydrogen-Ion Concentration / Q000187:drug effects; D007113:Immunity, Innate; D007473:Ion Channels / Q000037:antagonists & inhibitors*; D017136:Ion Transport / Q000187:drug effects; D009297:Nasal Mucosa / Q000187:drug effects / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D009298:Nasal Polyps; D009924:Organ Culture Techniques; D010256:Paranasal Sinuses / Q000473:pathology; D011522:Protons; D012220:Rhinitis / Q000150:complications / Q000276:immunology / Q000378:metabolism* / Q000503:physiopathology; D012852:Sinusitis / Q000150:complications / Q000276:immunology / Q000378:metabolism* / Q000503:physiopathology; D017967:Zinc Compounds / Q000494:pharmacology
chemical_list: D002712:Chlorides; C510235:HVCN1 protein, human; D007473:Ion Channels; D011522:Protons; D017967:Zinc Compounds; C016837:zinc chloride