The production of pro-inflammatory cytokines, such as interleukin-1 and tumor necrosis factor, is pivotal in the response to infection. However, overproduction of these cytokines might be detrimental. It has been suggested that (n-3) fatty acids suppress inflammation and ameliorate the course of infection by decreasing the production of pro-inflammatory cytokines. We here, review these effects. Use of (n-3) fatty acids induced moderate clinical improvements in rheumatoid arthritis, psoriasis and colitis, but not in systemic lupus erythematosus. Data on critically ill burn or postoperative cancer patients are still inconclusive. The (n-3) fatty acids markedly inhibited sterile inflammation in animal studies and improved survival in some experimental infections. T cell responses decreased in healthy volunteers but remained unchanged or increased in certain patient groups. The production of pro-inflammatory cytokines decreased in most human studies. The (n-3) fatty acids increased cytokine production capacity in mice. Differences in cytokine-producing cell types studied may account for these paradoxical responses in humans and mice. Although the increased cytokine production in mice is partly mediated by effects on prostaglandins, mechanisms of action in other species remain to be elucidated. The (n-3) fatty acids may be of moderate benefit in some chronic inflammatory diseases. Their therapeutic value and possible hazards in critically ill patients remain to be established.