Epidemiological data showed that total IgE and IL-4 levels in cigarette smokers were elevated, comparable to those in the asthmatics. The etiological agent(s) elevating IgE production are not clear. We evaluate whether tobacco polyphenols potentiate IgE production in a rodent model. Mice were fed with rutin or CGA in drinking water during antigen sensitization, followed by antigenic challenge i.p. in alum. CGA and rutin were also delivered in a bolus intraperitoneally or intranasally along with antigens during immunization. Antigen-specific IgE and IgG responses were measured. Enhancement of total IgE responses via i.p. and drinking routes can be achieved at concentrations as low as 0.1% CGA. Furthermore, IgG1 responses but not IgG2a and IgG2b were augmented, indicating a Th2 type of response by CGA. Moreover, both antigen-specific and serum IgE production can be achieved when CGA and antigenic challenges were delivered intranasally in the absence of alum. In contrast, nicotine does not enhance antigen-specific IgE production, and only marginally affects serum IgE levels. The more polarized Th2 development in CGA-treated mice may account for enhancement of both antigen-specific and total IgE responses. High levels of IL-4 but not IFN-γ or IL-12, were observed in antigen-challenged mesenteric lymph nodes (MLN) cultures from CGA-treated mice. In contrast, significant levels of IL-4, IL-12, and IFN-γ were observed in antigen-challenged cultures from nicotine-treated mice. This study shows that tobacco polyphenols, CGA and rutin potentiated IgE production in vivo. Polyphenolic antioxidants enhance Th2 development. We propose that IgE production and T cell dichotomy may be critically influenced by the redox microenvironment. Enhanced Th2 development and IgE production henceforth may counteract more severe Th1-mediated tissue damage triggered by environmental oxidative stress.
- Th2 dichotomy
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