Acceleration of SLE-like syndrome development in NZBxNZW F1 mice by beta-glucan. (April 2014)

• Record Type: Journal Article
• Authors: Fagone, P; Mangano, K; Mammana, S; Quattrocchi, C; Magro, G; Coco, M; Imene, S; Marco, R Di; Nicoletti, F
• Is Part Of: Lupus. Volume 23:Number 4(2014)
• Page Start: 407
• Page End: 411
• Publication Date: 2014-04
• Subjects: Anti-DNA antibodies -- nephritis -- renal lupus; Systemic lupus erythematosus -- Periodicals; 616.772005
• DOI: 10.1177/0961203314522333
• Languages: English
• ISSNs: 0961-2033

Abstract

Beta-glucans are naturally occurring polysaccharides that exert important immunostimulatory activities. In the present study, we evaluated whether beta-glucans could modulate the development and the course of systemic lupus erythematosus (SLE). To this aim, we employed the classical model of SLE represented by the F1 hybrid between the NZB and NZW mouse strains which develop severe lupus-like phenotypes comparable to that of SLE patients. The administration of beta-glucan was associated to a more aggressive development of the disease and a worse prognosis, as observed from the clinical, biochemical and histopathological data. This finding implies that restraint should be practised in the possible use of beta-glucans as immunomodulators in human therapy in the context of SLE.