Suppressive effect of environmental tobacco smoke on murine Th2 cell-mediated nasal eosinophilic inflammation.

Abstract

BackgroundEnvironmental tobacco smoke (ETS) exposure is recognized as a risk factor for the development of various respiratory diseases.ObjectiveIn this study, the effect of ETS on allergen-immunized and allergen-specific Th2 cell-transferred murine eosinophilic inflammation models and that of cigarette smoke extract (CSE) and nicotine on allergen-induced Th2 cell proliferation and interleukin (IL)-4 production were investigated.MethodsOvalbumin (OVA)-immunized and OVA-specific Th2 cell-transferred BALB/c mice were exposed to ETS and were challenged with OVA. Then, the number of inflammatory cells in the nasal mucosa and nasal hyperresponsiveness (NHR) were assessed. The effects of CSE and nicotine on the allergen-induced proliferative response of and IL-4 production by Th2 cells were determined in vitro.ResultsIn OVA-immunized and Th2 cell-transferred mice, allergen-induced NHR and nasal eosinophil infiltration were significantly suppressed by ETS exposure, whereas the accumulation of neutrophils was rather enhanced. Allergen-specific Th2 cell proliferation and IL-4 production were inhibited by coculture with CSE. The same effects were induced by nicotine, though the effect on proliferation was relatively weak.ConclusionRegardless of its harmful effect, ETS suppresses NHR, probably through the inhibition of Th2 cell responses.