Pro- and anti-inflammatory cytokines expression in rat's brain and spleen exposed to chronic mild stress: Involvement in depression

Stress-induced neuroinflammation is mediated by GSK3-dependent TLR4 signaling that promotes susceptibility to depression-like behavior

“…While there is no information regarding the cause of this differential inflammatory response to stress, previous studies have reported that inescapable foot or tail shocks do not increase IL-6 or IL-1 in the prefrontal cortex (Nguyen et al, 2000;Deak et al, 2003;Blandino et al, 2009). On the other hand, cytokines in the prefrontal cortex or cortex were reported to increase after acute social defeat stress (Audet et al, 2011), chronic restraint stress (Garate et al, 2013), and chronic mild stress (Garate et al, 2011;You et al, 2011). These disparate findings raise the possibility that stress induced by shock paradigms preferentially affect hippocampal cytokines whereas stress induced by non-shock paradigms affect cytokines in both the hippocampus and the prefrontal cortex.…”

“…Rodents exhibiting depression-like behaviors also have elevated brain cytokine levels (Goshen et al, 2008;Kreisel et al, 2014), and administration of inflammatory cytokines causes depressionlike behaviors in rodents (Bluthé et al, 2000;De la Garza et al, 2005;Dantzer and Kelley 2007;Palin et al, 2008;Fu et al, 2010). Acute inescapable tail shocks, acute or chronic restraint stress, and social defeat stress, all of which induce depressive-like behaviors in rodents, activate the inflammatory transcription factor nuclear factor-κB (NF-κB) and increase levels of the cytokines IL-1β, TNFα, IL-6 and IL-10 in rodent brains (Nguyen et al, 2000;Madrigal et al, 2002;O'Connor et al, 2003;Deak et al, 2003;Deak et al, 2005;Blandino et al, 2006;Blandino et al, 2009;Audet et al, 2011;Wohleb et al, 2011;You et al, 2011). In addition to inducing neuroinflammation, stress amplified the increases of inflammatory cytokines (e.g., IL-1β, TNFα) in rodent brains induced by peripheral administration of the inflammatory Toll-like receptor 4 (TLR4) agonist lipopolysaccharide (LPS) (Quan et al, 2001;Johnson et al, 2002;Johnson et al, 2003;Johnson et al, 2004;Munhoz et al, 2006;De Pablos et al, 2006;Frank et al, 2007;Espinosa-Oliva et al, 2009;Wohleb et al, 2012).…”

Salvianolic acid B ameliorates depressive-like behaviors in chronic mild stress-treated mice: involvement of the neuroinflammatory pathway

“…Growing evidence suggests that there is a causative link between depressive-like behaviors and life events, inflammation and apoptosis in the brain [37] . Our previous research indicated that the dysregulation of pro-and anti-inflammatory cytokines have a crucial role in the pathophysiology of depression [38] . Pro-inflammatory cytokines (TNF-α, IL-1β) or lipopolysaccharide-induced depressive-like behavior and neuroinflammatory reaction can be reversed by anti-inflammatory cytokines, such as TGF-β and IL-10 [39,40] .…”

Study of antidepressant effects of grape seed oil in male mice using tail suspension and forced swim tests

“…Studies have shown that most symptoms of chronic unpredictable stress-induced depression occur due to the impairment of neuroendocrine, anti-oxidant defense, and inflammatory systems (Eren et al, 2007;Mao et al, 200;Marks et al, 2009;You et al, 2011). A study by Schaalan et al (2011), reported neuroendocrine impairment and significant increase in serum adrenocorticotropin and corticosterone levels in mice exposed to chronic unpredictable stress (Schaalan and Nassar, 2011).…”

“…It was reported that the expression of proinflammatory cytokines such as TNF , interleukin-6, and interleukin-1 beta significantly increased in the brain and spleen of mice under chronic stress, and expression of anti-inflammatory cytokines such as TGFand interleukin-10 significantly decreased (You et al, 2011).…”