Peripheral chemokine levels in women with recurrent major depression with suicidal ideation

Abstract

The findings of this study indicated that the presence of recurrent MDD with suicidal ideation is associated with differences in inflammatory chemokines when compared to those without suicidal ideation.

Proteomics profiling reveals inflammatory biomarkers of antidepressant treatment response: Findings from the CO-MED trial

“…Hence, our findings suggest that Eotaxin-1 may be an easily detectable peripheral marker of synaptogenesis and/or effective antidepressant treatment. On the contrary, however, other studies have either found an association of Eotaxin-1 with more severe depression (as compared to healthy controls) (Maes et al, 1999) or a lack of association with MDD (Grassi-Oliveira et al, 2012; Magalhaes et al, 2014; Myung et al, 2016). The demographics of these studies largely differ from ours, however, as one is limited to young, unmedicated patients and another is limited to females, either of which may help explain the discrepancy in results.…”

“…The association of MDD with inflammation is also supported by the fact that IFN treatment of hepatitis C and certain types of cancers frequently induces depressive symptoms (Hauser et al, 2002). Grassi-Oliveira and colleagues have also reported that levels of certain chemokines (monocyte chemoattractant protein-1 [MCP-1/CCL-2] and RANTES/CCL5) are lower in serum samples from adults with MDD and suicidal ideation as compared to controls, while higher levels of Eotaxin-1/CCL-11 (further referred to as Eotaxin-1) are seen in those with MDD and suicidal ideation (Grassi-Oliveira et al, 2012), although neither study assessed changes with treatment.…”

Rapid Transport of CCL11 across the Blood-Brain Barrier: Regional Variation and Importance of Blood Cells

“…Adult neurogenesis is thought to be important in the preservation of cognitive function (Kempermann et al, 2004). Of note, other conditions associated with cognitive decline, such as obesity (Elias et al, 2003) and depression (Jorm, 2000), have also been associated with increased levels of CCL11 in the circulation (Vasudevan et al, 2006;Grassi-Oliveira et al, 2012). Although previous findings suggest that CCL11 from the circulation has direct effects on the neurogenic niche (Villeda et al, 2011), the mechanism by which CCL11 affects the brain has not been determined.…”

“…This indicates that the BBB could be an important regulatory interface for CCL11 levels in the brain, with potential effects on both adult neurogenesis and possibly other functions of CCL11 in the CNS that have yet to be defined. Increased circulating levels of CCL11 have been implicated in other diseases associated with aberrant CNS function, including Alzheimer disease (Leung et al, 2013), schizophrenia (Teixeira et al, 2008), and depression (Grassi-Oliveira et al, 2012). Elucidating roles for CCL11 function in the CNS may provide evidence for causal relationships between CCL11 elevations in blood and these diseases.…”

“…CCL11 has been implicated in a number of diseases that involve allergic eosinophilia, such as asthma, atopic dermatitis, and inflammatory conditions of the bowel (Rankin et al, 2000). Elevations in circulating CCL11 have also been reported in a variety of nonallergic conditions, including aging (Shurin et al, 2007;Villeda et al, 2011), obesity (Vasudevan et al, 2006), psychiatric disorders (Teixeira et al, 2008;Grassi-Oliveira et al, 2012), and cannabis use (Fernandez-Egea et al, 2013). Recently, it was shown that elevated circulating CCL11 can contribute to cognitive decline in aging by directly inhibiting adult hippocampal neurogenesis (Villeda et al, 2011).…”