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Genistein suppresses antigen-specific immune responses through competition with 17beta-estradiol for estrogen receptors in ovalbumin-immunized BALB/c mice.
Nutrition. 2006 Jul-Aug; 22(7-8):802-9.N

Abstract

OBJECTIVE

The aim of this study was to determine the effects of phytoestrogen genistein on antigen (Ag)-specific immune responses and elucidate the mechanisms underlying those effects.

METHODS

Ovalbumin (OVA)-immunized BALB/c mice were administered genistein for 35 d, and OVA-specific immune responses were examined by measuring OVA-specific proliferative responses, production of cytokines, and antibody responses. To assess the effect of genistein on antibody responses to thymus-independent Ag, mice were immunized with 2,4,6-trinitrophenyl (TNP)-Ficoll instead of OVA. Effect of genistein on the functions of CD11c(+) dendritic cells was also examined. Finally, to determine the contribution of estrogen receptor to genistein-mediated immune regulation, mice that had been administered genistein were treated with the estrogen receptor antagonist ICI 182,780 and OVA-specific proliferative responses were examined.

RESULTS

OVA-specific proliferative responses and interferon-gamma production levels were decreased in mice administered 20 mg/kg genistein compared with those in control mice without reduction in responses to anti-CD3 monoclonal (m)antibody. The level of OVA-specific immunoglobulin (Ig)G1 was also decreased in mice administered genistein. Levels of OVA-specific IgG2a and IgG2b production and interleukin-4 production in response to OVA were not significantly different but tended to decrease in genistein-treated mice. Genistein administration did not influence the TNP-specific IgM and IgG levels. Furthermore, genistein did not affect the Ag-presenting activity of CD11c(+) dendritic cells. Treatment with ICI 182,780 decreased OVA-specific proliferative responses, but genistein did not suppress these responses synergistically in mice treated with ICI 182,780.

CONCLUSIONS

The results of this study suggest that genistein suppresses Ag-specific immune responses. The mechanism underlying the suppression is responsible for the competition of genistein with endogenous 17beta-estradiol for estrogen receptors.

Authors+Show Affiliations

Department of International Nutrition, Institution of Health Bioscience, The University of Tokushima Graduate School, Tokushima, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16815494

Citation

Kogiso, Mari, et al. "Genistein Suppresses Antigen-specific Immune Responses Through Competition With 17beta-estradiol for Estrogen Receptors in Ovalbumin-immunized BALB/c Mice." Nutrition (Burbank, Los Angeles County, Calif.), vol. 22, no. 7-8, 2006, pp. 802-9.
Kogiso M, Sakai T, Mitsuya K, et al. Genistein suppresses antigen-specific immune responses through competition with 17beta-estradiol for estrogen receptors in ovalbumin-immunized BALB/c mice. Nutrition. 2006;22(7-8):802-9.
Kogiso, M., Sakai, T., Mitsuya, K., Komatsu, T., & Yamamoto, S. (2006). Genistein suppresses antigen-specific immune responses through competition with 17beta-estradiol for estrogen receptors in ovalbumin-immunized BALB/c mice. Nutrition (Burbank, Los Angeles County, Calif.), 22(7-8), 802-9.
Kogiso M, et al. Genistein Suppresses Antigen-specific Immune Responses Through Competition With 17beta-estradiol for Estrogen Receptors in Ovalbumin-immunized BALB/c Mice. Nutrition. 2006 Jul-Aug;22(7-8):802-9. PubMed PMID: 16815494.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Genistein suppresses antigen-specific immune responses through competition with 17beta-estradiol for estrogen receptors in ovalbumin-immunized BALB/c mice. AU - Kogiso,Mari, AU - Sakai,Tohru, AU - Mitsuya,Kaori, AU - Komatsu,Tatsushi, AU - Yamamoto,Shigeru, PY - 2005/11/16/received PY - 2006/03/20/revised PY - 2006/04/11/accepted PY - 2006/7/4/pubmed PY - 2006/12/9/medline PY - 2006/7/4/entrez SP - 802 EP - 9 JF - Nutrition (Burbank, Los Angeles County, Calif.) JO - Nutrition VL - 22 IS - 7-8 N2 - OBJECTIVE: The aim of this study was to determine the effects of phytoestrogen genistein on antigen (Ag)-specific immune responses and elucidate the mechanisms underlying those effects. METHODS: Ovalbumin (OVA)-immunized BALB/c mice were administered genistein for 35 d, and OVA-specific immune responses were examined by measuring OVA-specific proliferative responses, production of cytokines, and antibody responses. To assess the effect of genistein on antibody responses to thymus-independent Ag, mice were immunized with 2,4,6-trinitrophenyl (TNP)-Ficoll instead of OVA. Effect of genistein on the functions of CD11c(+) dendritic cells was also examined. Finally, to determine the contribution of estrogen receptor to genistein-mediated immune regulation, mice that had been administered genistein were treated with the estrogen receptor antagonist ICI 182,780 and OVA-specific proliferative responses were examined. RESULTS: OVA-specific proliferative responses and interferon-gamma production levels were decreased in mice administered 20 mg/kg genistein compared with those in control mice without reduction in responses to anti-CD3 monoclonal (m)antibody. The level of OVA-specific immunoglobulin (Ig)G1 was also decreased in mice administered genistein. Levels of OVA-specific IgG2a and IgG2b production and interleukin-4 production in response to OVA were not significantly different but tended to decrease in genistein-treated mice. Genistein administration did not influence the TNP-specific IgM and IgG levels. Furthermore, genistein did not affect the Ag-presenting activity of CD11c(+) dendritic cells. Treatment with ICI 182,780 decreased OVA-specific proliferative responses, but genistein did not suppress these responses synergistically in mice treated with ICI 182,780. CONCLUSIONS: The results of this study suggest that genistein suppresses Ag-specific immune responses. The mechanism underlying the suppression is responsible for the competition of genistein with endogenous 17beta-estradiol for estrogen receptors. SN - 0899-9007 UR - https://www.unboundmedicine.com/medline/citation/16815494/Genistein_suppresses_antigen_specific_immune_responses_through_competition_with_17beta_estradiol_for_estrogen_receptors_in_ovalbumin_immunized_BALB/c_mice_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0899-9007(06)00175-4 DB - PRIME DP - Unbound Medicine ER -