Objective To investigate the effects of H1R antagonists on the inflammative adhesion mechanism of airway inflammation in asthmatic guinea pigs. Methods The guinea pigs were divided into 3 groups. Group 1 was treated with loratadine (2mg/kg·d-1); Group 2 with normal saline (1 ml/d); and Group 3 with ketotifen (0.1 mg/kg·d-1). In 3 groups, the following tests were performed: (a) the sICAM-1, sP-selectin, IL-8 and eosinophilic cationic protein (ECP) values both in plasm (or serum) and bronchoalveolar lavage fluid (BALF) were mesured by ELISA; (b) the expressions of intercellular adhesion molecule-1 (ICAM-1) and IL-8 on the bronchial epithelial cells were measured by immuno-histochemistry staining; (c) the lung functions (Vt, Cdyn, RL) were tested. Results (a) Except for IL-8 in plasm, the values of sICAM-1, sP-selectin and ECP were inhibited by H1R antagonists (loratadine and ketotifen) both in the plasm (or serum) and BALF of asthmatic animals (P < 0.05) . (b) The expressions of ICAM-1 and IL-8 on the bronchial epithelial cells and pulmonary vascular endothelial cells in asthmatic animals were down-regulated both in ketotifen and loratadine groups especially in loratrdine group (P < 0.05). (c) The lung functions (Vt, Cdyn, RL) of the asthmatic animals were improved by 2 kinds of H1R antagonists (P <0.05). Conclusion ICAM-1 is the natural ligand of leukocyte functional associated antigen-1 (LFA-1), a widely expression integrin, and present also on eosinophils surface, the present study clearly demonstrated that H1R antagonists especially for loratadine decreased different components of the allergic airway inflammation especially significant reduction of ICAM-1 expression on target cells. Since it has been widely demonstrated that the ICAM-1 is deeply involved in cell-to-cell interaction during allergic inflammation of asthma, administration of loratadine may be necessary to suppress the late allergic reaction (LAR) of asthma.