Cytokines such as interleukin (IL)-4, IL-5 and IL-13 mainly produced by CD4+ type 2 helper T lymphocytes (Th2 cells) have an important role in pathophysiology of allergic airway inflammation. Therefore, modulation of Th2 cells may offer a novel therapeutic approach to control allergic asthma. It has been suggested that n-3 PUFA can be used as preventive or therapeutic strategy to control allergic asthma. However, mechanisms by which n-3 PUFA modulates this disease are not fully understood. Here, the effects of elevated n-3 PUFA on OVA-induced airway inflammation were investigated using Fat-1 transgenic mice which can convert n-6 PUFA to n-3 PUFA endogenously. First, this study tested whether Fat-1 expression modulates CD4+ T cell activation, proliferation, and differentiation in vitro and found that Fat-1 expression attenuated all of these CD4+ T cell responses. When Fat-1 mice were sensitized and challenged with OVA, these mice showed significantly reduced inflammatory cell recruitment into airway, lower levels of Th2 cytokines, mucin production and eotaxin in brochoalveolar lavage (BAL) and lung tissues. OVA-specific IgE were also significantly lower in Fat-1 mice. Furthermore, suppressed CD4+ T cell activation and differentiation were also observed in Fat-1 mice. Taken together, these results demonstrate that elevated n-3 PUFA play a protective role in airway inflammation by modulating CD4+ T cell activation and differentiation in Fat-1 mice.
- Copyright © 2013 by The American Association of Immunologists, Inc.