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  • Meeting abstract
  • Open Access

Basic and clinical immunology – 3021. Inhibitory action of levocetirzine hydrochloride on eosinophil actication in vitro

  • 1,
  • 2 and
  • 2
World Allergy Organization Journal20136:480

  • Published:


  • Rhinitis
  • Effector Cell
  • Allergic Rhinitis
  • Allergic Disease
  • Factor Production


Histamine H1 receptor antagonists are used for the treatment of allergic disorders such as allergic rhinitis and atopic allergy with remarkable success. However, the influence of antihistamines on the function of eosinophils, which are the most important final effector cells in allergic diseases, is not well understood.


The influence of histamine H1 receptor antagonists on eosinophil functions was examined through the choice of levocetirizine hydrochloride (LH) in vitro and in vivo.


BALB/c male mice (5 weeks of age) were intraperitoneally infected with 500 Mesocestoides cortii larvae. These mice were then treated with LH at a single dose of 0.1 mg/kg once a day, which was started on the day of infection. The percent of peripheral blood eosinophils and IgE levels were examined 21 days after infection. In the second experiments, eosinophils obtained from mice infected with M cortii were sensitized with M.cortii-specific IgE, and these sensitized eosinophils were stimulated with 10 ng/ml of M. cortii excretory antigen in the presence of LH for 24 h. MIP-1β, LTC4and RANTES levels in culture supernatants were examined by ELISA.


Oral administration of LH could not suppress both peripheral blood eosinophila and IgE hyper-production, which were observed in mice infected with M cortii. The addition of LH into cell cultures could suppress the ability of eosinophils to produce MIP-1β, LTC4 and RANTES, which were increased by SCF stimulation. The minimum concentrations of LH, which caused significant suppression of factor production, were 1.0μM for MIP-1β and LTC4, and 0.5 μM for RANTES.


These results may suggest that LH exerts inhibitory effects on eosinophil activation and results in favorable modification of clinical status of pollinosis patients.

Authors’ Affiliations

Department of Otorhinolaryngology, School of Medicine, Showa University, Tokyo, Japan
Physiology, Showa University, Japan


© Furuta et al; licensee BioMed Central Ltd. 2013

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.