Neural mechanisms linking social status and inflammatory responses to social stress.
|Title||Neural mechanisms linking social status and inflammatory responses to social stress.|
|Publication Type||Journal Article|
|Year of Publication||2016|
|Authors||Muscatell KA, Dedovic K, Slavich GM, Jarcho MR, Breen EC, Bower JE, Irwin MR, Eisenberger NI|
|Journal||Soc Cogn Affect Neurosci|
|Date Published||2016 Jun|
Social stratification has important implications for health and well-being, with individuals lower in standing in a hierarchy experiencing worse outcomes than those higher up the social ladder. Separate lines of past research suggest that alterations in inflammatory processes and neural responses to threat may link lower social status with poorer outcomes. This study was designed to bridge these literatures to investigate the neurocognitive mechanisms linking subjective social status and inflammation. Thirty-one participants reported their subjective social status, and underwent a functional magnetic resonance imaging scan while they were socially evaluated. Participants also provided blood samples before and after the stressor, which were analysed for changes in inflammation. Results showed that lower subjective social status was associated with greater increases in inflammation. Neuroimaging data revealed lower subjective social status was associated with greater neural activity in the dorsomedial prefrontal cortex (DMPFC) in response to negative feedback. Finally, results indicated that activation in the DMPFC in response to negative feedback mediated the relation between social status and increases in inflammatory activity. This study provides the first evidence of a neurocognitive pathway linking subjective social status and inflammation, thus furthering our understanding of how social hierarchies shape neural and physiological responses to social interactions.
|Alternate Journal||Soc Cogn Affect Neurosci|
|PubMed Central ID||PMC4884319|
|Grant List||K08 MH103443 / MH / NIMH NIH HHS / United States |
P30 AG028748 / AG / NIA NIH HHS / United States