Seite - (000140) - in Biomedical Chemistry: Current Trends and Developments

facilitating cognitive flexibility in the orbitofrontal cortex (Donegan, 2014). A depressive syndrome can be associated with cytokine administration, typically during IFN-α treatment of hepatitis C or malignant melanoma (Bonaccorso, 2000; Dieperink, 2004; Hauser, 2002; Kraus, 2003; Schaefer, 2004), the psychopathological presentation can include changes in mood or cognition, psychomotor retardation, fatigability, sleep disturbances and decreased appetite (Capuron & Miller, 2004; Loftis, 2006; Raison, 2006). Dysregulation of the T-cell arm of the immune system has corroborated the role of immunomediators in depression (Kronfol & Remick, 2000; Pavon, 2006). Evidence supporting both the predominance of T-cells Th1 or Th2 have increased and the balance of these two subtypes of cytokine-producing T cells Th1/Th2 regulates the immune response to pathogens. These two main lineages of cells differentiate from naïve CD4+ T lymphocytes and have distinct cytokine profiles. Th1 patterns are related to increased inflammation and autoimmune conditions, and the production of IFN-γ, TNF-α or IL-1; conversely, Th2 patterns are related to allergic responses and asthma, and the production of IL-6, IL-10 or IL-13 (Kimball, 2005; Pavon, 2006; Scott, 2007). Data from our lab supports that there is an imbalance of Th1/Th2 activities with a predominance of Th1 in MDD; we found increased chemokine CXCL10/IP10 levels, which decreased with antidepressant treatment, and decreased IL-13 levels; although no distinct Th1 or Th2 cytokine patterns was found in our MDD patients (Wong, 2008). Nevertheless, different types of MDD may exhibit divergent immune profiles, and decreased Th1 activation has been described in melancholic depressed patients, which is accompanied by a marked HPA axis activation. Non-melancholic MDD patients show increased inflammation features with elevated monocyte count and levels of IL-1ß and α2-macroglobulin (Kaestner, 2005; Rothermundt, 2001). Post- partum depression also shows a predominance of Th1 activation (Maes, 2002; Ostensen, 2005), and symptoms of anxiety and depression in the early post-partum period are related to increased levels of pro- inflammatory cytokine IL-8 (Maes, 2002).