Writing in the Proceedings of the National Academy of Sciences, Professor Edward Dennis and his colleagues from the University of California, San Diego, said their findings also suggest it could be possible to boost the effects of omega-3’s and ‘short-circuit’ inflammation before it begins.
"There have been tons of epidemiological studies linking health benefits to omega-3 oils, but not a lot of deep science," said Dennis. "This is the first comprehensive study of what fish oils actually do inside a cell."
The research leader said this ability to unravel what is happening inside cells when treated with omega-3 is "ground-breaking."
"We've been able to look inside a cell, see what fish oils do and determine that the process of inflammation at this level may be manipulatable," said Dennis."Now, we need to learn if we can fine-tune that process so we can use omega-3 oils to reduce the production of pro-inflammatory prostaglandins and boost the production of anti-inflammatory resolvins."
The observations made by the team, may also be helpful in identifying potential adverse effects from taking fish oil, he said – noting that since omega-3 fatty acids possess overlapping functions with COX inhibitor drugs (which have well-known side effects) using both in combination can produce unexpected consequences.
Study details
Dennis and his colleagues fed mouse macrophage cells (part of the immune system) three different kinds of fatty acid: eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA) and arachidonic acid (AA).
After supplementation the scientists stimulated them to produce an inflammatory response – finding that that omega-3 fatty acids inhibited the cyclooxygenase (COX) enzyme, which produces the prostaglandin hormones that spark inflammation. Dennis noted that this action is similar to what happens when a person takes an aspirin, which disrupts the COX-2 signaling pathway, thus reducing inflammation and pain.
“Using a targeted lipidomics approach, we observed that Toll-like receptor 4 and purinergic receptor activation of supplemented cells leads to the release of 22-carbon fatty acids that potently inhibit cyclooxygenase pathways,” explained the researchers.
They added that the 22-carbon fatty acid (docosapentaenoic acid - DPA) was responsible for cyclooxygenase inhibition after EPA supplementation, “offering fresh insights into how EPA exerts anti-inflammatory effects indirectly through elongation to 22-carbon DPA.”
Source: Proceedings of the National Academy of Sciences
Published online ahead of print, doi:10.1073/pnas.1200189109
“Omega-3 fatty acids cause dramatic changes in TLR4 and purinergic eicosanoid signalling”
Authors: Paul C. Norris, Edward A. Dennis
