چکیده (انگلیسی):

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-kB 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-kB inhibitor dramatically reduced ICAM-1 expression in IL-33-treated
BMMCs, suggesting the involvement of NF-kB 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 tryptasepositive
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.