TNF-α-mediated anxiety in a mouse model of multiple sclerosis

Modulatory effect of celastrol on Th1/Th2 cytokines profile, TLR2 and CD3+ T-lymphocyte expression in a relapsing–remitting model of multiple sclerosis in rats

“…To achieve this, a model of relapsing-remitting EAE was established in this work. Typically, it exhibited motor deficit within 9-12 days post-immunization and relapsed after the re-challenge at the 35th day post-immunization in accordance to that described in previous studies (O'Brien et al, 2001;Constantinescu et al, 2011;Haji et al, 2012). As reported previously, the re-challenge by a booster dose of MBP exhibited higher NO levels than immunization with a primary dose only (O'Brien et al, 1999) that seems to render the model more vulnerable to the inhibitory effect of aminoguanidine and induction of relapse.…”

Effects of Centrally Administered Etanercept on Behavior, Microglia, and Astrocytes in Mice Following a Peripheral Immune Challenge

“…This role of TNFa is supported by previous studies where genetic knockout of TNF-a reduced anxiety-like behavior in young mice (Camara et al, 2013), while central blockade reduced experimental autoimmune encephalitis -induced anxiety in mice (Haji et al, 2012). Additionally, TNF-a antagonists reduced anxiety in chronic pain models in mice after peripheral administration , and this was supported by decreased anxiety observed in RA patients after anti-TNF-a treatment (Uguz et al, 2009).…”

“…Additionally, TNF-a antagonists reduced anxiety in chronic pain models in mice after peripheral administration , and this was supported by decreased anxiety observed in RA patients after anti-TNF-a treatment (Uguz et al, 2009). Haji et al (2012) showed that the release of TNF-a from activated microglia altered excitatory transmission within the striatum promotes the development of anxiety-like behavior, whereas etanercept decreased decay time and duration of mini excitatory postsynaptic currents, indicating a reduction in glutamatergic signalling. Other potential mechanisms whereby TNF-a may induce the development of anxietylike behavior include the stimulation of microglia to release glutamate causing neurotoxicity by cell death (Takeuchi et al, 2006) and by silencing cell survival signals (Tamminga, 1998;Venters et al, 2000).…”

Differential roles of resident microglia and infiltrating monocytes in murine CNS autoimmunity

“…Numerous studies found TNF-α to be detrimental in EAE, although it was also reported to be associated with decreased clinical symptoms [88]. Moreover, TNF-α was associated with anxiety behavior in MOG-immunized mice [89]. IL-1β was also studied extensively in inflammatory disorders and is considered one of the most important transducers of inflammation, by activation of the NF-κB cascade [90].…”