Tissue Transglutaminase Can Be Involved in Airway Inflammation of Toluene Diisocyanate-Induced Occupational Asthma Gyu-Young Hur & Sung-Ho Kim & Sang Myun Park & Young-Min Ye & Cheol-Woo Kim & An-Soo Jang & Choon-Sik Park & Chein Soo Hong & Hae-Sim Park Received: 16 March 2009 / Accepted: 10 June 2009 / Published online: 27 June 2009 # Springer Science + Business Media, LLC 2009 Abstract Background This study was conducted to evaluate whether tissue transglutaminase (tTG) may be involved in airway inflammation of toluene diisocyanate-induced occupational asthma (TDI-OA). Methods We enrolled 93 patients with TDI-OA, 177 asymptomatic exposed subjects, 43 patients with allergic asthma, and 70 unexposed normal controls. The prevalence of serum immunoglobulin G (IgG) to tTG in the TDI-OA group (20.2%) was significantly higher than that in the three other groups (P <0.001). Results TDI-OA patients with serum IgG to tTG had significantly lower methacholine PC 20 values (P <0.02) and significantly higher prevalence of specific immuno- globulin E to vapor type TDI–human serum albumin conjugate (P <0.01; r 2 =0.411, P <0.05). TDI exposure could increase tTG activity via reactive oxygen species (ROS) production, which was found to cross-link with cytokeratin 19 on immunoblot analysis. Conclusion Therefore, TDI exposure may activate tTG via ROS-mediated mechanism in the airway epithelium leading to persistent airway inflammation in TDI-OA patients. Keywords Occupational asthma . specific immunoglobulin E . toluene diisocyanate . transglutaminase Introduction Toluene diisocyanate (TDI) exposure is the most com- mon cause of occupational asthma (OA) worldwide [1, 2]; in Korea, its prevalence is 2–13% in exposed workers [3–5]. Although many researchers have investigated its pathogenic mechanism, it is still not fully understood. However, previous studies detected a significant increase in the level of serum-specific immunoglobulin E (IgE) after the application of a vapor type TDI–human serum albumin (HSA) conjugate, indicating that IgE may play a role in TDI-induced OA (TDI-OA) [6]. An immunohisto- J Clin Immunol (2009) 29:786–794 DOI 10.1007/s10875-009-9314-8 Gyu-Young Hur and Sung-Ho Kim equally contributed to this work. G.-Y. Hur Department of Internal Medicine, Korea University College of Medicine, Seoul, South Korea S.-H. Kim : Y.-M. Ye : H.-S. Park (*) Department of Allergy and Rheumatology, Ajou University School of Medicine, San-5, Wonchon-dong, Youngtong-gu, Suwon 443-721, South Korea e-mail: hspark@ajou.ac.kr S. M. Park Pharmacology and Chronic Inflammatory Disease Research Center, Ajou University School of Medicine, Suwon, South Korea C.-W. Kim Department of Internal Medicine, Inha University College of Medicine, Incheon, South Korea A.-S. Jang : C.-S. Park Department of Internal Medicine, Soonchunhyang University Hospital, Bucheon, South Korea C. S. Hong Department of Internal Medicine, Yonsei University School of Medicine, Seoul, South Korea