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Effects of n-3 PUFA on the CD4+ type 2 helper T-cell-mediated immune responses in Fat-1 mice

Authors

  • Hyun-Young Jang,

    1. Department of Biochemistry and Research Institute for Endocrine Sciences, Chonbuk National University Medical School, Jeonju, Jeonbuk, Republic of Korea
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  • Kyu Lim,

    1. Department of Biochemistry and Cancer Research Institute, College of Medicine, Chungnam National University, Daejeon, Republic of Korea
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  • Sang-Myeong Lee,

    1. Division of Biotechnology, College of Environmental and Bioresource Sciences, Chonbuk National University, Iksan, Jeonbuk, Republic of Korea
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  • Byung-Hyun Park

    Corresponding author
    1. Department of Biochemistry and Research Institute for Endocrine Sciences, Chonbuk National University Medical School, Jeonju, Jeonbuk, Republic of Korea
    • Correspondence: Dr. Byung-Hyun Park, Department of Biochemistry and Research Institute for Endocrine Sciences, Chonbuk National University Medical School, 567 Baekje-daero, Deokjin-gu, Jeonju, Jeonbuk, Republic of Korea

      E-mail: bhpark@jbnu.ac.kr

      Fax: +82-63-274-9833

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Abstract

Scope

It has been suggested that n-3 PUFA can be used as a preventive or therapeutic strategy to control allergic asthma. But little is known about the exact mechanisms by which n-3 PUFA modulates it. Here, the effects of elevated n-3 PUFA on ovalbumin (OVA) induced airway inflammation were investigated using Fat-1 transgenic mice that can convert n-6 PUFA to n-3 PUFA endogenously.

Methods and results

First, we tested whether Fat-1 expression modulates CD4+ T-cell activation, proliferation, and differentiation in vitro and found that the Fat-1 expression attenuated all of these CD4+ T-cell responses by suppression of T-cell receptor mediated signaling and cytokine-mediated phosphorylation of STATs. When the Fat-1 mice were sensitized and challenged with the OVA, they showed a significant decrease in the recruitment of inflammatory cells into airway, the production of Th2 cytokines, eotaxin, and mucin in the lung, and the concentration of OVA-specific IgE in the serum. Furthermore, the differentiation of CD4+ T cells into Th2 was also decreased in the spleen of Fat-1 mice.

Conclusion

Our results showed that an elevated level of n-3 PUFA was effective in preventing allergic airway inflammation by modulating the activation and differentiation of CD4+ T cells in Fat-1 mice.

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