Abstract
Both high fat diet and obesity have been linked to impaired cell‐mediated immune response. Blueberry, rich in antioxidant phytochemicals, has been shown to impact biologic functions in several tissues. However, no information is available on immune cells. We investigated whether blueberry consumption affects immune response in obese mice induced by high fat diet. C57BL/6 mice were fed one of the 3 diets: low fat (LF), high fat (HF), or high fat plus 2% (w/w) blueberry (HF+B), for 8 or 12 wk. After 8 and 12 wk, both HF groups had higher body weight than the LF group and at 12 wk HF+B group had a higher body weight than the HF group. Lymphocyte proliferation responding to T cell mitogen Con A or PHA, or anti‐CD3/CD28 was not different at 8 wk but significantly lower at 12 wk in both HF groups compared to the LF group (HF>HF+B>LF). At 8 wk, the LF group had a lower IL‐4 and higher prostaglandin (PG)E2 production compared to both HF groups. At 12 wk, compared to LF group, HF but not HF+B group had lower IL‐4 and interferon‐γ production and contrary to reports in other tissues, both HF groups had lower production of IL‐1β, IL‐6, and TNF‐α indicating that obesity‐induced inflammation is tissue specific. While PGE2 production was similar between LF and HF groups, it tended to be lower in HF+B group. No difference in IL‐2 and IL‐10 production was found at either time points. In summary, HF impairs T cell proliferative response and addition of blueberries does not intervene in this effect. The high fat‐induced T cell‐suppressive effect may be related to the lower production of inflammatory cytokines. Supported by USDA #58‐1950‐7‐707 and the US Highbush Blueberry Council.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have