title: IL-33 promotes ICAM-1 expression via NF-kB in murine mast cells.
abstract: BACKGROUND
  IL-33, a member of the IL-1 cytokine family, binds to heterodimeric receptors ST2 and IL-1 receptor accessory protein, and activates Th2-type immune responses. The signals from the ST2 receptor are mediated by the two major pathways, including AP-1 and NF-κB molecules. The present study examined whether IL-33 induced ICAM-1 expression in bone marrow-derived mast cells (BMMCs).
  
  
  METHODS
  BMMCs from C57BL/6J mice, cultured in media containing IL-3 (20 ng/ml), were treated with IL-33 (50 ng/ml) for up to 72 h. ICAM-1 expression with mRNA and protein, degranulation of siRNA ICAM-1 transfected BMMCs, and cell adhesion were analyzed. In the in vivo part of the experiment rIL-33 (500 ng) was injected intradermally into the ear pinnae of mice and any resulting pathological changes were assessed.
  
  
  RESULTS
  ICAM-1 mRNA expression was increased one hour after IL-33 stimulation while ICAM-1 protein attained maximum expression levels 24 h after IL-33 stimulation. Moreover, IL-33-treated BMMCs showed increased cell adhesion to the LFA-1-coated plate. However, siRNA ICAM-1 transfected BMMCs did not affect Ag/IgE-mediated degranulation level compared to the wild control siRNA. Pre-treatment with a NF-κB inhibitor dramatically reduced ICAM-1 expression in IL-33-treated BMMCs, suggesting the involvement of NF-κB in the process. In vivo study, at 6 h after IL-33 treatment, MCs histologically showed up-regulated ICAM-1 expression though the number of tryptase-positive cells did not change.
  
  
  CONCLUSIONS
  These data suggest that MCs increase ICAM-1 expression and activate LFA-1 positive cells in the early phase of skin inflammation in response to IL-33.
authors.affiliation: Department of Dermatology, Tokyo Medical University, Tokyo, Japan.
authors.forename: Takafumi
authors.initials: T
authors.lastname: Numata
authors.affiliation: Department of Dermatology, Tokyo Medical University, Tokyo, Japan. Electronic address: tomonobu@tokyo-med.ac.jp.
authors.forename: Tomonobu
authors.initials: T
authors.lastname: Ito
authors.affiliation: Department of Dermatology, Tokyo Medical University, Tokyo, Japan.
authors.forename: Tatsuo
authors.initials: T
authors.lastname: Maeda
authors.affiliation: Department of Dermatology, Tokyo Medical University, Tokyo, Japan.
authors.forename: Chizu
authors.initials: C
authors.lastname: Egusa
authors.affiliation: Department of Dermatology, Tokyo Medical University, Tokyo, Japan.
authors.forename: Ryoji
authors.initials: R
authors.lastname: Tsuboi
mesh_terms: D000818:Animals; D015550:Cell Degranulation / Q000187:drug effects / Q000276:immunology; D002478:Cells, Cultured; D005786:Gene Expression Regulation / Q000187:drug effects*; D018799:Intercellular Adhesion Molecule-1 / Q000235:genetics*; D000067596:Interleukin-33 / Q000378:metabolism* / Q000494:pharmacology; D008407:Mast Cells / Q000187:drug effects / Q000276:immunology / Q000378:metabolism*; D051379:Mice; D016328:NF-kappa B / Q000378:metabolism*; D034622:RNA Interference; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D034741:RNA, Small Interfering / Q000235:genetics; D012867:Skin / Q000187:drug effects / Q000276:immunology / Q000378:metabolism
chemical_list: D000067596:Interleukin-33; D016328:NF-kappa B; D012333:RNA, Messenger; D034741:RNA, Small Interfering; D018799:Intercellular Adhesion Molecule-1
keywords: Adhesion; ICAM-1; IL-33; Mast cells; NF-kB