FRIDAY, June 27 (HealthDay News) -- Two proteins involved in the recognition of pathogens are also involved in the inflammatory response in a mouse model of arthritis, according to study findings published online June 23 in the Proceedings of the National Academy of Sciences Early Edition.
Leo A.B. Joosten, Ph.D., from Radboud University Nijmegen Medical Centre in the Netherlands, and colleagues investigated the role of Nod1 and Nod2 in a mouse model of acute joint inflammation induced by injection of Streptococcus pyogenes cell wall fragments and in human peripheral blood mononuclear cells (PBMCs) with defects in Nod1 and Nod2.
The researchers found that mice lacking the Nod2 gene had reduced joint inflammation and protection against cartilage damage, while mice lacking Nod1 had enhanced joint inflammation and cartilage damage. After exposure to bacterial cell wall fragments, human PBMCs carrying a Nod2 mutation had reduced production of the proinflammatory cytokines TNFα and IL-1β compared with normal PBMCs, while PBMCs carrying a Nod1 mutation had enhanced production of proinflammatory cytokines.
"These data indicate that
Nod1 and Nod2 have different functions in controlling inflammation, and that intracellular Nod1-Nod2 interactions may determine the severity of arthritis in this experimental model," Joosten and colleagues conclude.
Abstract
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