title: Passive sensitization increases histamine-stimulated calcium signaling and NF-kappaB transcription activity in bronchial epithelial cells.
abstract: OBJECTIVE
  To find out if the two aspects of asthma (chronic airway inflammation and bronchial hyperresponsiveness) are related to hypersensitivity of calcium signaling in bronchial epithelial cells.
  
  
  METHODS
  Porcine bronchial epithelial cells (PBEC) were divided into sensitized (S) and non-sensitized (N) groups. In group S, the cells were preincubated with serum from ovalbumin sensitized guinea pigs. In group N, the cells were preincubated with serum from nonsensitized guinea pigs. Single cell calcium imaging and ELISA-based NF-kappaB activity were used to evaluate the histamine-stimulated intracellular free calcium level and NF-kappaB activity, respectively.
  
  
  RESULTS
  First, 0.1 micromol/L histamine could induce [Ca(2+)](i) oscillations in PBEC of group S, but not in group N. Second, 1 micromol/L histamine could induce [Ca(2+)](i) oscillations of PBEC in both group S and group N. The [Ca(2+)](i) oscillation frequency of PBEC was significantly higher in group S than in group N, though the [Ca(2+)](i) oscillation amplitude showed no difference between the two groups. Finally, when 10 micromol/L histamine was used to stimulate PBEC, a transient initial increase followed by a sustained elevation (FSE) of [Ca(2+)](i) was observed in PBEC in both groups. The amplitude of the FSE of [Ca(2+)](i) in PBEC was significantly higher in group S than in group N. The subsequent NF-kappaB activity was in accordance to the calcium oscillation frequency evoked by histamine, but not to the amplitude.
  
  
  CONCLUSIONS
  It was suggested that the increased sensitivity of calcium signaling in bronchial epithelial cells might contribute to the exorbitant inflammation or increased susceptibility in asthmatic airway epithelial cells.
authors.affiliation: Department of Pathophysiology, Tongji Medical College, Huazhong University of Science and Technology; Key Laboratory of Pulmonary Disease of Ministry of Health of China, Wuhan 430030, China. jinsi@mails.tjmu.edu.cn
authors.forename: Si
authors.initials: S
authors.lastname: Jin
authors.forename: Dan
authors.initials: D
authors.lastname: Tian
authors.forename: Jian-Guo
authors.initials: JG
authors.lastname: Chen
authors.forename: Li-Ping
authors.initials: LP
authors.lastname: Zhu
authors.forename: Sheng-Yuan
authors.initials: SY
authors.lastname: Liu
authors.forename: Di-Xun
authors.initials: DX
authors.lastname: Wang
mesh_terms: D000818:Animals; D001249:Asthma / Q000139:chemically induced / Q000378:metabolism*; D001980:Bronchi / Q000166:cytology; D020013:Calcium Signaling / Q000187:drug effects*; D004305:Dose-Response Relationship, Drug; D004847:Epithelial Cells / Q000166:cytology / Q000378:metabolism*; D006168:Guinea Pigs; D006632:Histamine / Q000494:pharmacology*; D007116:Immunization, Passive; D008297:Male; D016328:NF-kappa B / Q000378:metabolism*; D010047:Ovalbumin; D011897:Random Allocation; D013552:Swine
chemical_list: D016328:NF-kappa B; D006632:Histamine; D010047:Ovalbumin