Open AccessVitamin E uncouples joint destruction and clinical inflammation in a transgenic mouse model of rheumatoid arthritis
Author(s) -
Bandt Michel De,
Grossin Maggy,
Driss Fathi,
Pincemail Joël,
BabinChevaye Catherine,
Pasquier Catherine
Publication year - 2002
Publication title -
arthritis & rheumatism
Language(s) - English
Resource type - Journals
eISSN - 1529-0131
pISSN - 0004-3591
DOI - 10.1002/art.10085
Subject(s) - rheumatoid arthritis , medicine , vitamin e , inflammation , immunology , arthritis , genetically modified mouse , vitamin , vitamin d and neurology , tumor necrosis factor alpha , nod mice , transgene , interleukin , cytokine , endocrinology , antioxidant , disease , autoimmune disease , biology , biochemistry , gene
Objective Reactive oxygen species are thought to play a role in rheumatoid arthritis (RA) in humans. We postulated that antioxidant treatment could have a beneficial effect in this disease. We therefore investigated the effects of vitamin E in the transgenic KRN/NOD mouse model of RA. Methods Mice were treated by gavage with oral vitamin E (α‐tocopherol). Clinical, histologic, and biochemical parameters were assessed for 6 weeks. Results Vitamin E treatment did not modify the clinical features of the disease (date of onset or disease intensity, as measured by the articular index), but it did prevent joint destruction, as measured by qualitative and semiquantitative analyses. Redox status did not differ between treated and control mice. White blood cell chemiluminescence was higher in transgenic KRN/NOD mice than in controls, but vitamin E treatment attenuated this difference. Vitamin E treatment of the transgenic animals led to a significant decrease in the levels of interleukin‐1β (IL‐1β) but not tumor necrosis factor α. Conclusion Vitamin E seems to uncouple joint inflammation and joint destruction in this model of RA, with a beneficial effect on joint destruction. Since many investigations are currently in progress to evaluate the benefit of interventions targeted toward anti‐IL‐1β, our findings suggest opportunities of therapeutic interest in human RA.