The Feeding of [beta]-Carotene Down-Regulates Serum IgE Levels and Inhibits the Type I Allergic Response in Mice

• Published in: Biological & pharmaceutical bulletin Vol. 27; no. 7; p. 978
• Main Authors: Sato, Yuji, Akiyama, Hiroshi, Suganuma, Hiroyuki, Watanabe, Takahiro, H. Nagaoka, Megumi, Inakuma, Takahiro, Goda, Yukihiro, Maitani, Tamio
• Format: Journal Article
• Language: English
• Published: Tokyo Japan Science and Technology Agency 01.07.2004
• ISSN: 0918-6158; 1347-5215

Feed containing β-carotene was administered orally to BALB/c mice immunized intraperitoneally with ovalbumin (OVA) for approximately 1 month. The titers of OVA-specific IgE, OVA-specific IgG1 and OVA-specific IgG2a in the mouse sera were determined. The OVA-specific IgE titer and OVA-specific IgG1 titer by mice fed β-carotene were significantly inhibited. On the other hand, the OVA-specific IgG2a titer in mice fed β-carotene was significantly greater than those of control mice. The OVA-specific IgE suppression of β-carotene feeding was dose-dependent. We also examined the effect of fed β-carotene on active systemic anaphylaxis. Feeding β-carotene to mice immunized with OVA inhibited the immediate reduction of the body temperature induced by antigen stimulation. Furthermore, the increase in serum histamine in the mice fed β-carotene under active systemic anaphylaxis was lower than in controls. We then examined the pattern of cytokine production by spleen cells from mice followed by restimulation with OVA in vitro. The spleen cells from the mice fed β-carotene produced more IFN-γ, IL-12 and IL-2 than those from the control group. In contrast, the spleen cells from the mice fed β-carotene produced less IL-4, IL-5, IL-6, IL-10 than those from the control group. Furthermore, analysis of IFN-γ mRNA levels of the splenocytes using the real-time quantitative RT-PCR technique revealed higher levels in the splenocytes from the mice fed β-carotene. These findings suggest that feeding β-carotene improves the helper T cell (TH)1-TH2 balance, inhibiting specific IgE and IgG1 production and antigen-induced anaphylactic response.