Effects of suplatast tosilate on airway inflammation and airway hyperresponsiveness

T. Horiguchi, S. Tachikawa, M. Handa, K. Hanazono, R. Kondo, A. Ishibashi, K. Banno

Research output: Contribution to journalArticlepeer-review

21 Citations (Scopus)


Suplatast tosilate (IPD®) is a Th2 cytokine inhibitor that lowers the titer of the IgE antibody through specific inhibition of the production of IL (interleukin)-4 and IL-5 by T cells and inhibits tissue infiltration by eosinophils. In this clinical trial, suplatast tosilate (300 mg/day) was administered orally for 4 weeks to 25 patients (13 patients with atopic asthma, 12 patients with nonatopic asthma) whose bronchial asthma was staged in step 1 or step 2 according to the Guidelines for Prevention and Management of Bronchial Asthma, 1998. Before and after administration, the parameters of airway inflammation, that is, peripheral blood eosinophils count, serum level of eosinophil cationic protein (ECP), ECP level in induced sputum, airway hyperresponsiveness (Dmin), and morning peak expiratory flow (PEF), were measured. The peripheral blood eosinophil count, serum level of ECP, and ECP level in induced sputum decreased significantly. Of these parameters, the ECP level in induced sputum was the most sensitive. Furthermore, suplatast tosilate significantly inhibited Dmin. These results were especially significant in patients with atopic asthma. Suplatast tosilate was considered to have inhibited airway eosinophilic inflammation through decreases in peripheral blood eosinophils counts and in ECP levels in induced sputum, which resulted in inhibition of airway hyperresponsiveness.

Original languageEnglish
Pages (from-to)331-336
Number of pages6
JournalJournal of Asthma
Issue number4
Publication statusPublished - 24-07-2001

All Science Journal Classification (ASJC) codes

  • Pediatrics, Perinatology, and Child Health
  • Immunology and Allergy
  • Pulmonary and Respiratory Medicine


Dive into the research topics of 'Effects of suplatast tosilate on airway inflammation and airway hyperresponsiveness'. Together they form a unique fingerprint.

Cite this