Abstract
A social signal transduction theory of depression has been proposed that states that exposure to social adversity alters the immune response and these changes mediate symptoms of depression such as anhedonia and impairments in social behavior The exposure of maternal rats to the chronic social stress (CSS) of a male intruder depresses maternal care and impairs social behavior in the F1 and F2 offspring of these dams. The objective of the present study was to characterize basal peripheral levels of several immune factors and related hormone levels in the adult F2 offspring of CSS exposed dams and assess whether changes in these factors are associated with previously reported deficits in allogrooming behavior. CSS decreased acid glycoprotein (α1AGP) and intercellular adhesion molecule-1 (ICAM-1) in F2 females, and increased granulocyte macrophage-colony stimulating factor (GM-CSF) in F2 males. There were also sex dependent changes in IL-18, tissue inhibitors of metalloproteinases 1 (TIMP-1), and vascular endothelial growth factor (VEGF). Progesterone was decreased and alpha melanocyte stimulating hormone (α-MSH) was increased in F2 males, and brain-derived neurotrophic factor (BDNF) was decreased in F2 females. Changes in α1AGP, GM-CSF, progesterone, and α-MSH were correlated with decreased allogrooming in the F2 offspring of stressed dams. These results support the hypothesis that transgenerational social stress affects both the immune system and social behavior, and also support previous studies on the adverse effects of early life stress on immune functioning and stress associated immunological disorders, including the increasing prevalence of asthma. The immune system may represent an important transgenerational etiological factor in disorders which involve social and/or early life stress associated changes in social behavior, such as depression, anxiety, and autism, as well as comorbid immune disorders. Future studies involving immune and/or endocrine assessments and manipulations will address specific questions of function and causation, and may identify novel preventative measures and treatments for the growing number of immune mediated disorders.
Highlights
A social signal transduction theory of depression has been proposed that states that exposure to social adversity, especially during early life, alters immune responses, and these changes mediate depression symptoms such as anhedonia and impaired social behavior (Slavich and Irwin, 2014)
IL-18 [F(1, 45) = 10.3, p < 0.01, Figure 2D] and tissue inhibitors of metalloproteinases 1 (TIMP-1) [F(1, 45) = 14.9, p < 0.01, Figure 2E] levels were higher in F2 males compared to F2 females, where levels of vascular endothelial growth factor (VEGF) were lower in F2 males [F(1, 45) = 32.0, p < 0.01, Figure 2F]
While there were overall sex differences in IL-18, TIMP-1, and VEGF, these factors were not affected by chronic social stress (CSS)
Summary
A social signal transduction theory of depression has been proposed that states that exposure to social adversity, especially during early life, alters immune responses, and these changes mediate depression symptoms such as anhedonia and impaired social behavior (Slavich and Irwin, 2014). Maternal immune activation induces adverse changes in offspring social behavior (Hodes et al, 2014; Machado et al, 2015). Exposure to early life stress alters the systemic immune response and behavior (O’Mahony et al, 2009, 2011) and there is recent evidence that inflammatory factors (IL-1 and IL-6) increase vulnerability to stress related disorders and are associated with impairments in social behavior (Hodes et al, 2014; Wood et al, 2014). A robust social stressor often used in rodent studies, increases cytokine secretion (Powell et al, 2009), deficient maternal care alters immune associated gene expression (Cole et al, 2012), and it is postulated that inflammation may mediate the adverse effects of early life stress on mental health (Danese et al, 2007; Carpenter et al, 2010)
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
