title: Human airway smooth muscle cells express eotaxin in response to signaling following mast cell contact.
abstract: BACKGROUND
  Asthma is a chronic inflammatory disease of the airways. Mast-cell (MC)-derived cytokines may mediate both airway inflammation and remodeling. It has also been shown that airway smooth muscle cells (ASMC) can be a source of proinflammatory cytokines. In the human airways, MC-ASMC cell interactions may have pivotal effects on modulating inflammation.
  
  
  OBJECTIVE
  We wanted to know whether the production of eotaxin, an important proinflammatory cytokine, through a cell-to-cell contact mechanism of human ASMC activation by MC was mediated by p38 MAPK.
  
  
  METHODS
  We cocultured normal humanASMC with a human MC line (HMC-1) and assayed for the production of eotaxin.
  
  
  RESULTS
  When cultured together, human ASMC and HMC-1 contact induced eotaxin secretion. Separation of HMC-1 and human ASMC by a porous membrane inhibited this induction. Coculturing of human ASMC with HMC-1 induced increased expression of eotaxin gene mRNA. HMC-1-derived cellular membranes caused an increase in eotaxin production in human ASMC. Activation of p38 MAPK was also seen in cocultures by Western blot, whereas eotaxin production in cocultures was significantly inhibited by the p38 inhibitor SB203580.
  
  
  CONCLUSIONS
  These novel studies reveal the importance of cell-to-cell interactions in the complex milieu of airway inflammation.
authors.affiliation: Department of Respiratory Disease, Renmin Hospital, Wuhan University, Wuhan, China. cutliu@sohu.com
authors.forename: L
authors.initials: L
authors.lastname: Liu
authors.forename: J
authors.initials: J
authors.lastname: Yang
authors.forename: Y
authors.initials: Y
authors.lastname: Huang
mesh_terms: D015153:Blotting, Western; D001980:Bronchi / Q000166:cytology; D002478:Cells, Cultured; D054413:Chemokine CCL11; D019742:Chemokines, CC / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D018920:Coculture Techniques; D003907:Dexamethasone / Q000494:pharmacology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005938:Glucocorticoids / Q000494:pharmacology; D006801:Humans; D007093:Imidazoles / Q000494:pharmacology; D008407:Mast Cells / Q000378:metabolism*; D032389:Myocytes, Smooth Muscle / Q000378:metabolism*; D011725:Pyridines / Q000494:pharmacology; D012333:RNA, Messenger / Q000032:analysis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D048051:p38 Mitogen-Activated Protein Kinases / Q000037:antagonists & inhibitors / Q000378:metabolism
chemical_list: C515456:CCL11 protein, human; D054413:Chemokine CCL11; D019742:Chemokines, CC; D004791:Enzyme Inhibitors; D005938:Glucocorticoids; D007093:Imidazoles; D011725:Pyridines; D012333:RNA, Messenger; D003907:Dexamethasone; D048051:p38 Mitogen-Activated Protein Kinases; C093642:SB 203580