Histamine release and inflammatory cell infiltration in airway Mucosa in methylene diphenyl diisocyanate (MDI)-induced occupational asthma.

INTRODUCTION

Although methylene diphenyl diisocyanate (MDI) is widely used in industries, there have been few studies of the pathogenic mechanisms of MDI-induced occupational asthma (MDI-OA).

METHODS

We performed immunohistochemical analyses, measured inflammatory mediators and cytokines, and quantified histamine release (HR) from peripheral basophils in MDI-OA patients. Thirteen MDI-exposed workers (five MDI-OA, two MDI-induced esoinophilic bronchitis, and six asymptomatic exposed controls, AEC) were enrolled.

RESULTS AND DISCUSSION

Immunochemical analyses indicated significantly increased anti-eosinophilic cationic protein-stained cells in MDI-OA patients as compared with controls (P < 0.05). Sputum eosinophil cationic protein levels were increased after MDI-specific inhalation challenge test in MDI-OA/EB patients (P < 0.02). Sputum eosinophil counts were highly correlated with IL-8 and MMP-9 levels (P < 0.05 and P < 0.01, respectively). Basophil HR was significantly increased in MDI-OA patients after stimulations with anti-IgG4 and MDI-human serum albumin conjugates (both P < 0.05). Eosinophil activation is a major feature of airway inflammation in MDI-OA patients. Increased HR by MDI may contribute to the pathogenic mechanisms of MDI-OA.