Background Allergic airway eosinophilia is suppressed by cysteinyl leukotriene (CysLT) receptor (CysLT₁ receptor) antagonists in several species including humans and guinea‐pigs, suggesting that CysLTs are directly or indirectly involved in induction of the response.

Objective We examined the effect of CysLT antagonists (pranlukast and MCI‐826) on antigen inhalation‐induced eosinophilia in peripheral blood and lung, and on IL‐5 activity in serum during late increase of airway resistance (late asthmatic response, LAR) in sensitized guinea‐pigs.

Methods Guinea‐pigs inhaled ovalbumin (OVA) + Al(OH)₃ and OVA mists alternately for sensitization and challenge, respectively, once every 2 weeks. At the fifth challenge, the effects of CysLT antagonists and an anti‐IL‐5 antibody (TRFK‐5) on the occurrence of LAR, and blood and lung eosinophilia, which appeared at 5 h after challenge, were examined. The time‐course of IL‐5 activity in the serum after the challenge was evaluated by measuring in vitro‘eosinophil survival prolongation activity’. The influence of CysLT antagonists on IL‐5 activity was assessed.

Results CysLT antagonists and TRFK‐5 completely abolished blood and lung eosinophilia. LAR was suppressed by both MCI‐826 and TRFK‐5 by 40–50%. Sera obtained from sensitized, challenged animals 3 h and 4 h after challenge induced an obvious prolongation of eosinophil survival. The activity of the sera was completely neutralized by prior exposure to TRFK‐5, suggesting that it reflected IL‐5 activity. Increased IL‐5 activity in the serum was inhibited by both pranlukast and MCI‐826 by over 90%.

Conclusions CysLTs produced after antigen provocation sequentially induced IL‐5 production from some immune component cells via CysLT₁ receptor activation. Thus, it is likely that CysLTs indirectly cause antigen‐induced eosinophilia through IL‐5 production.