title: The effect of N-acetylcysteine on Clara cells and Clara cell 16 kDa protein in a murine model of allergen-induced airway inflammation.
abstract: OBJECTIVE
  The aim of this study was to investigate the number of Clara cells and the production and secretion of Clara cell 16 kDa protein (CC16) in a murine model of allergen-induced airway inflammation, as well as the effects of N-acetylcysteine (NAC) on CC16 and Clara cell numbers, in order to determine the mechanism of the anti-inflammatory effect of NAC.
  
  
  METHODS
  BALB/c mice were divided into control, ovalbumin (OVA) and NAC groups. An allergen-induced airway inflammation model (OVA group) was established by sensitizing and challenging mice with OVA. NAC was administered as an oral treatment. The number of Clara cells and the production of CC16 were determined by immunohistochemistry. The CC16 levels in bronchoalveolar lavage fluid (BALF) were determined by Western blotting.
  
  
  RESULTS
  The proportion of Clara cells in terminal and respiratory bronchioles significantly decreased in the OVA group compared to the control group (P < 0.01). NAC treatment did not change the proportion of Clara cells in the OVA group (P > 0.05). CC16 production by Clara cells in the OVA groups was significantly lower than that of the control group (P < 0.01), but was elevated following NAC treatment (P < 0.05). The CC16 level in BALF of the OVA group was lower than that of the control group (P < 0.01), but was elevated by NAC treatment (P < 0.05). NAC reduced the total number of white cells and the percentage of eosinophils in BALF. Moreover, it inhibited airway inflammation.
  
  
  CONCLUSIONS
  The number of Clara cells and the production and secretion of CC16 were reduced in a murine model of allergen-induced airway inflammation. Antioxidants can enhance the expression of CC16, which might be a mechanism by which they suppress airway inflammation.
authors.affiliation: Department of Respiratory Medicine, Changhai Hospital, Shanghai, China. xmnie@hotmail.com
authors.forename: Xiaomeng
authors.initials: X
authors.lastname: Nie
authors.forename: Qiang
authors.initials: Q
authors.lastname: Li
authors.forename: Gang
authors.initials: G
authors.lastname: Cai
authors.forename: Yimin
authors.initials: Y
authors.lastname: Dai
authors.forename: Jun
authors.initials: J
authors.lastname: Zhang
mesh_terms: D000111:Acetylcysteine / Q000008:administration & dosage / Q000494:pharmacology*; D000284:Administration, Oral; D000818:Animals; D015153:Blotting, Western; D001980:Bronchi / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D016535:Bronchial Hyperreactivity / Q000276:immunology / Q000378:metabolism / Q000517:prevention & control*; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D002452:Cell Count; D004195:Disease Models, Animal; D005260:Female; D007150:Immunohistochemistry; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D010047:Ovalbumin / Q000276:immunology; D014598:Uteroglobin / Q000378:metabolism*
chemical_list: C556390:Scgb1a1 protein, mouse; D010047:Ovalbumin; D014598:Uteroglobin; D000111:Acetylcysteine