Effects of n‐3 PUFA on the CD4+ type 2 helper T‐cell‐mediated immune responses in Fat‐1 mice. Issue 2 (9th September 2013)
- Record Type:
- Journal Article
- Title:
- Effects of n‐3 PUFA on the CD4+ type 2 helper T‐cell‐mediated immune responses in Fat‐1 mice. Issue 2 (9th September 2013)
- Main Title:
- Effects of n‐3 PUFA on the CD4+ type 2 helper T‐cell‐mediated immune responses in Fat‐1 mice
- Authors:
- Jang, Hyun‐Young
Lim, Kyu
Lee, Sang‐Myeong
Park, Byung‐Hyun - Abstract:
- <abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <sec id="mnfr2076-sec-0010" sec-type="section"> <title>Scope</title> <p>It has been suggested that <italic>n</italic>‐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 <italic>n</italic>‐3 PUFA modulates it. Here, the effects of elevated <italic>n</italic>‐3 PUFA on ovalbumin (OVA) induced airway inflammation were investigated using Fat‐1 transgenic mice that can convert <italic>n</italic>‐6 PUFA to <italic>n</italic>‐3 PUFA endogenously.</p> </sec> <sec id="mnfr2076-sec-0020" sec-type="section"> <title>Methods and results</title> <p>First, we tested whether Fat‐1 expression modulates CD4<sup>+</sup> T‐cell activation, proliferation, and differentiation in vitro and found that the Fat‐1 expression attenuated all of these CD4<sup>+</sup> 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<sup>+</sup> T cells into Th2 was also decreased in the spleen of Fat‐1 mice.</p> </sec> <sec id="mnfr2076-sec-0030" sec-type="section"><abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <sec id="mnfr2076-sec-0010" sec-type="section"> <title>Scope</title> <p>It has been suggested that <italic>n</italic>‐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 <italic>n</italic>‐3 PUFA modulates it. Here, the effects of elevated <italic>n</italic>‐3 PUFA on ovalbumin (OVA) induced airway inflammation were investigated using Fat‐1 transgenic mice that can convert <italic>n</italic>‐6 PUFA to <italic>n</italic>‐3 PUFA endogenously.</p> </sec> <sec id="mnfr2076-sec-0020" sec-type="section"> <title>Methods and results</title> <p>First, we tested whether Fat‐1 expression modulates CD4<sup>+</sup> T‐cell activation, proliferation, and differentiation in vitro and found that the Fat‐1 expression attenuated all of these CD4<sup>+</sup> 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<sup>+</sup> T cells into Th2 was also decreased in the spleen of Fat‐1 mice.</p> </sec> <sec id="mnfr2076-sec-0030" sec-type="section"> <title>Conclusion</title> <p>Our results showed that an elevated level of <italic>n</italic>‐3 PUFA was effective in preventing allergic airway inflammation by modulating the activation and differentiation of CD4<sup>+</sup> T cells in Fat‐1 mice.</p> </sec> </abstract> … (more)
- Is Part Of:
- Molecular nutrition & food research. Volume 58:Issue 2(2014:Feb.)
- Journal:
- Molecular nutrition & food research
- Issue:
- Volume 58:Issue 2(2014:Feb.)
- Issue Display:
- Volume 58, Issue 2 (2014)
- Year:
- 2014
- Volume:
- 58
- Issue:
- 2
- Issue Sort Value:
- 2014-0058-0002-0000
- Page Start:
- 365
- Page End:
- 375
- Publication Date:
- 2013-09-09
- Subjects:
- Food -- Biotechnology -- Periodicals
Food -- Microbiology -- Periodicals
Nutrition -- Periodicals
Food -- Toxicology -- Periodicals
Nutrition -- Periodicals
Food Microbiology -- Periodicals
Food Technology -- Periodicals
Molecular Biology -- Periodicals
664.0705 - Journal URLs:
- http://onlinelibrary.wiley.com/ ↗
- DOI:
- 10.1002/mnfr.201300194 ↗
- Languages:
- English
- ISSNs:
- 1613-4125
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 5900.817992
British Library DSC - BLDSS-3PM
British Library HMNTS - ELD Digital store - Ingest File:
- 4093.xml