Omega-3 Rich Diet Seen to Have ‘Potent’ Effects in Treating a Mouse Model of Rheumatoid Arthritis

Omega-3 Rich Diet Seen to Have ‘Potent’ Effects in Treating a Mouse Model of Rheumatoid Arthritis

Rheumatoid arthritis (RA) may be effectively treated with the lipid mediator resolvin D1, a metabolite of omega-3 fatty acids, according to a study that found a pronounced easing of the disease in mice after treatment. The study, “Proresolving and cartilage-protective actions of resolvin D1 in inflammatory arthritis,” was published in JCI Insight.

RA is a chronic autoimmune disease characterized by the accumulation of inflammatory cells within the fluid of the joints, leading to joint damage. Chronic inflammatory diseases such RA often persist due to an inability to stop the inflammation. Current RA treatments are largely preventive, and depend on an early diagnose that maintains joint integrity by limiting inflammation before the disease progresses. Only rarely is a treatment able to reverse joint damage.

Dietary supplementation with fish oils is known to reduce joint pain in RA patients, although the underlying mechanisms are not well-understood. Researchers led by Mauro Perretti, with the William Harvey Research Institute in London, fed omega-3–enriched food to mice with inflammatory arthritis and compared them to animals given a standard died. Results revealed this special diet reduced arthritis. Moreover, the team identified elevated levels of resolvin D1 in mice fed diets with omega-3.

Inflammation resolution is mediated by the production of endogenous proresolving mediators, but their identity and mechanisms of action are still largely unknown. Resolvin D1 was found to abolish the migration of neutrophils — major immune players in inflammation — toward a chemotactic stimuli. Consistently, treatment with 17R-RvD1, a molecule with higher stability than resolvin D1 but that retains its biological function, significantly eased the severity of arthritis and leukocyte infiltration, by increasing protective proresolving lipid mediators (SPM).

In addition, researchers also found that 17R-RvD1 enhanced the expression of genes associated with the synthesis of cartilage matrix, with consequent cartilage repair and reduced factors linked to joint damage.

“The results we present here using synthetic RvD1 as a prototype therapeutic tool from the SPM portfolio, a choice dictated by detection of this bioactive mediator in mouse and human joints, opens the opportunity to exploit this line of research for innovative therapeutic strategies in RA that combine potent anti-inflammatory with tissue-protective properties,” the researchers concluded.

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