Nitric Oxide and TNFα Effects in Experimental Autoimmune Encephalomyelitis Demyelination

Abstract

The involvement of inducible nitric oxide synthase (iNOS), which plays various roles in the progression of autoimmune diseases, was studied in iNOS knockout (KO) mice and wild-type (WT) controls with respect to experimental autoimmune encephalomyelitis (EAE). The iNOS (KO) mice presented a less severe form of the disease than the WT control mice. Although the levels of TNFα decreased in the periphery in both groups, an increase in the number of TNFα-positive cells was detected in the central nervous system during the acute phase of EAE in the WT mice, but not in the KO mice. These findings suggest that NO and TNFα contribute to the pathogenesis of acute EAE.

Liposomal Encapsulation of Glucocorticoids Alters Their Mode of Action in the Treatment of Experimental Autoimmune Encephalomyelitis

“…Production of NO, which exerts deleterious effect in EAE and MS (36,37), and MHC II surface expression, which is FIGURE 7. Liposome-encapsulated prednisolone reduces the expression of proinflammatory cytokines and chemokines, but increases M2-associated genes in the spinal cord.…”

Distinct role of nitric oxide and peroxynitrite in mediating oligodendrocyte toxicity in culture and in experimental autoimmune encephalomyelitis

“…Studies have shown that pharmacological inhibitors or targeted gene deletion of iNOS and gp91phox are protective against reactive microglia-induced toxicity to neurons and OLs in culture (Xie et al, 2002;Li et al, 2005). Although a number of studies have shown that deletion of iNOS potentiates the disease severity of EAE (Fenyk-Melody et al, 1998;Sahrbacher et al, 1998;van der Veen et al, 2000van der Veen et al, , 2004Hultqvist et al, 2004;Farias et al, 2007), the contribution of NADPH oxidase in the pathogenesis of EAE has not been well elucidated. It has been reported that targeted gene deletion of p47phox can either increase or decrease the severity of several autoimmune diseases (van der Veen et al, 2000(van der Veen et al, , 2004Hultqvist et al, 2004).…”

Interferon β-1a Induces Tumor Necrosis Factor Receptor 1 but Decreases Tumor Necrosis Factor Receptor 2 Leukocyte mRNA Levels in Relapsing-Remitting Multiple Sclerosis

“…During the acute phase of experimental autoimmune encephalomyelitis (EAE) in mice, an increase in the number of tumor necrosis factor (TNF)-␣ -positive cells is detected in the central nervous system (CNS) [1] . The tissue-specifically expressed TNF receptors 1 and 2 (TNF-R1, TNFRSF1A; TNF-R2, TNFRSF1B) mediate apoptosis or inflammation [2] .…”