Research data from Kumamoto University, Department of Neurology update understanding of amyloidosis

12-19-2006

Fresh data on amyloidosis are presented in the report "FK506 inhibits murine AA amyloidosis: possible involvement of T cells in amyloidogenesis." In this recent study, researchers in Honjo, Japan conducted a study "To determine the possibility that T cells represent a potential target for therapy in AA amyloidosis. AA amyloidosis was induced in C3H/HeN mice by concomitant administration of AgNO3 and amyloid-enhancing factor (AEF)."

"Mice injected with AgNO3 and AEF received intraperitoneal injections of FK506 (2-200 microg/day). The degree of splenic amyloid deposition was determined by Congo red staining. Serum amyloid A (SAA), interleukin 1beta (IL-1beta), IL-6, and tumor necrosis factor-a concentrations were measured by ELISA. AA amyloidosis was also induced in ICR mice by injection of Freund's complete adjuvant (FCA) and Mycobacterium butyricum without AEF. ICR mice injected with FCA and M. butyricum also received intraperitoneal injections of FK506 (200 microg/day) to eliminate the possibility that FK506 action might depend upon AEF activity in the amyloid formation. Amyloid deposition was also induced with and without AEF in severe combined immunodeficient (SCID) mice and nude mice to clarify the role of T cells in the mechanism of amyloid formation in AA amyloidosis. FK506 treatment significantly reduced the amount of amyloid deposition and incidence of amyloidosis without reducing serum SAA and proinflammatory cytokine levels in the murine AA amyloidosis models with and without AEF. SCID mice and nude mice showed resistance to development of AA amyloidosis. Our findings may provide a new therapeutic strategy for amyloidosis," wrote M. Ueda and colleagues, Kumamoto University, Department of Neurology.

The researchers concluded: "The results suggested that T cells may play an important role in the mechanism of amyloid formation in AA amyloidosis."

Ueda and colleagues published their study in the Journal of Rheumatology (FK506 inhibits murine AA amyloidosis: possible involvement of T cells in amyloidogenesis. Journal of Rheumatology, 2006;33(11):2260-70).

For more information, contact M. Ueda, Graduate School of Medical Sciences, Dept. of Neurology, Kumamoto University, 1-1-1 Honjo, Kumamoto 860-0811, Japan.

Publisher contact information for the Journal of Rheumatology is: J Rheumatol Publ Co., 920 Yonge St., Suite 115, Toronto, Ontario M4W 3C7, Canada.

Keywords: Japan, Honjo, Amyloidosis, FK506, Nephrology, Rheumatology, Severe Combined Immunodeficiency, Therapy, Treatment.

This article was prepared by Drug Law Week editors from staff and other reports. Copyright 2006, Drug Law Week via NewsRx.com.