TRPM2 channels are not required for acute airway inflammation in OVA-induced severe allergic asthma in mice
1 Laboratory for Cellular and Molecular Signaling, Center for Biomedical Research at The Queen’s Medical Center and John A. Burns School of Medicine, University of Hawai’i, 1301 Punchbowl St, Honolulu, HI, 96813, USA
2 University of Hawaii Cancer Center, Honolulu, HI, 96813, USA
Journal of Inflammation 2013, 10:19 doi:10.1186/1476-9255-10-19Published: 1 May 2013
Airway inflammation and asthma have been linked to oxidative stress and the melastatin-related transient receptor potential cation channel, member 2 (TRPM2), which can be activated by reactive oxygen species (ROS), has emerged as a potential therapeutic target for inflammatory diseases.
Using TRPM2 deficient (TRPM2-/-) mice, we investigated whether the TRPM2 ion channel, which mediates calcium (Ca2+) influx and lysosomal Ca2+ release, plays a role in the pathophysiology of severe allergic asthma in mouse.
Severe allergic asthma was initiated in wild type (WT) and TRPM2-/- mice by repeated sensitization with ovalbumin (OVA)/aluminum hydroxide on Days 0, 7 and 14, followed by intranasal challenge on Days 21, 22 and 23. Mice were investigated for the presence of airway responsiveness, airway inflammation, production of allergen-specific antibodies, cytokine response and lung pathology.
The absence of TRPM2 channels has no obvious effect on major etiologic markers of severe allergic asthma in this mouse model. Neither airway resistance nor mucus production are affected in TRPM2-/- mice. TRPM2 channel ablation also does not alter airway inflammation or immunocyte infiltration and does not affect antibody response or cytokine levels.
TRPM2 is not required for airway inflammation in OVA-induced severe allergic asthma in mice. Accordingly, TRPM2 might not be a suitable therapeutic target for airway inflammation caused by allergens in humans.