Background: Inflammatory bowel diseases (IBD) are immune-mediated diseases, which are common in western industrialized countries while they are uncommon in developing countries. The hygiene hypothesis suggests that the loss of exposure to helminthes such as Echinococcus granulosus engendered a development of IBD. This parasite causes cystic hydatid disease which is endemic in Algeria. Previous data reported that helminthes reduce inflammatory process in experimental colitis. The aim of our study is to investigate the immuno-modulatory effect of the secondary infection with Echinococcus granulosus on Nitric Oxide (NO) production in Dextran Sulfate Sodium (DSS) induced colitis model. Materials and Methods: A group of Swiss mice is infected intraperitoneally (i.p) with 200 µl of a suspension containing 2000 viable protoscoleces of Echinococcus granulosus. After 3 months of infection, experimental colitis is induced in infected and uninfected mice by dissolving DSS in their drinking water for 7 days and then were sacrificed. We estimated disease activity index (DAI) which took into account body weight, stool consistency and gross bleeding. Nitric oxide (NO), is determined to investigate the inflammatory response. Results: Our results show that the disease activity index (DAI) of colitis increased at slow pace in the infected mice which developed cysts in comparison to the uninfected mice. In addition, a significant decrease in nitric oxide production is observed in plasma of infected mice. Conclusion: Our experiments suggest a potential immuno-modulatory effect of Echinococcus granulosus on Dextran Sulfate Sodium (DSS) experimental colitis by nitric oxide (NO) down-modulation.