TY - JOUR
T1 - Polyphenolic antioxidants enhance IgE production
AU - Gong, Jian
AU - Liu, Fu-Tong
AU - Chen, Swey Shen
PY - 2004
Y1 - 2004
N2 - 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.
AB - 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.
KW - Antioxidant
KW - IgE
KW - Polyphenol
KW - Th2 dichotomy
UR - http://www.scopus.com/inward/record.url?scp=4644241830&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=4644241830&partnerID=8YFLogxK
U2 - 10.1081/IMM-120037603
DO - 10.1081/IMM-120037603
M3 - Article
C2 - 15495789
AN - SCOPUS:4644241830
VL - 33
SP - 295
EP - 307
JO - Immunological Investigations
JF - Immunological Investigations
SN - 0882-0139
IS - 3
ER -