NEW YORK (Reuters Health), Apr 29 - Mucosal administration of alpha-fodrin, a common actin-binding cytoskeletal protein, can inhibit the progression of Sjögren's syndrome (SS) in an experimental mouse model, according to a study by Chinese researchers published online in Arthritis Research & Therapy on April 18.
Earlier studies by these and other researchers had implicated alpha-fodrin as an autoantigen in Sjögren's syndrome.
Dr. Jing He and colleagues at Peking University Medical School, Beijing, administered alpha-fodrin to 16 female nonobese diabetic mice, half of which received 1 µg intranasally every other day, the other half receiving 10 µg. Two control groups of eight mice each received phosphate-buffered saline 10 µl or glutathione-S-transferase 10 µg.
The levels of antialpha-fodrin antibodies were lower in the mice immunized with alpha-fodrin (p < 0.05), though there was no significant dose effect shown by the two experimental groups.
In addition, the volume of water intake by the immunized mice was significantly lower than that by the control mice, showing that the administration of alpha-fodrin helped to maintain function of the salivary glands.
Histological examination of the animals' salivary glands showed decreased lymphocytic infiltration in the immunized mice relative to the control groups.
"The mechanism by which this treatment protects against impaired gland activity has not yet been elucidated," the researchers write. "We propose that multiple low doses of autoantigen may result in the generation of antigen-specific regulatory cells, which in turn secrete immunosuppressive cytokines such as TGF-beta upon restimulation with the antigen."
By Scott Baltic
Arthritis Research & Therapy 2008;10.
Last Updated: 2008-04-29 17:15:15 -0400 (Reuters Health)
