Silencing ICAM-1 reduces the adhesion of vascular endothelial cells in mice with immunologic contact urticaria.

Objective: Immunologic contact urticaria (ICU) is an immediate response of wheal caused by various contactants in vulnerable individuals, with undefined pathogenesis.

Methods: In the present study, we aim to explore the effects of intercellular cell adhesion molecule-1 (ICAM-1) gene silencing by RNA inference (RNAi) on vascular endothelial cells (VECs) adhesion molecule expression and cell-cell adhesion in ICU mice. Sixty BALB/c mice were selected, among which 48 mice were used for establishment of ICU models. VECs from normal and ICU mice were grouped into different groups. Expressions of ICAM-1, eosinophilic cationic protein (ECP), total immunologlobulin E (tIgE), L-selectin (CD62L), integrin, alpha L (CD11a) in tissues and cells were evaluate by RT-qPCR and western blotting. Cell proliferation was evaluated by MTT assay and EdU staining and cell adhesive function by cell-cell adhesion assay.

Results: Compared with normal mice, ICU mice had increased expressions of ICAM-1, ECP, tIgE, CD62L, and CD11a.ICAM-1 gene silencing decreased expressions of ECP, tIgE, CD62L, and CD11a, enhanced cell proliferation, and more activity in cell adhesion.

Conclusion: These findings indicate that RNAi-mediated gene silencing of ICAM-1 may decrease VECs adhesion expression and reduce cell-cell adhesion in mice with ICU.