Neurocognitive Pathways and Social Rejection-Induced Inflammatory Responses

psychological stress

A recent study published in the Proceedings of the National Academy of Sciences of the USA (PNAS) indicates that a social stressor involving social-evaluative threat and rejection elicits significant increases in inflammatory activity, as indexed by both soluble receptor for tumor necrosis factor-alpha (sTNFalphaRII) and interleukin (IL)-6.

Recent evidence indicates that psychological stress may affect the onset or progression of several common human diseases at least in part by up-regulating acute or chronic inflammatory processes.

Among various stressors, it appears that social stress is a particularly strong trigger of inflammation, but the neurocognitive pathways that underlie this effect remain unknown. Prior research has shown that an acute episode of social rejection is linked to activation of specific brain regions such as the dorsal anterior cingulate cortex (dACC) and the anterior insula.

In the PNAS study, George Slavich and colleagues from the University of California, Los Angeles report that greater activity in the dACC and bilateral anterior insula was associated with greater sTNFaRII responses, whereas greater activity in the right anterior insula was marginally related to increases in IL-6.

According to the authors this indicates that neural responses to social rejection are associated with potentiated inflammatory responses to an episode of acute social stress. This is consistent with previous studies showing that greater social rejection-induced dACC activity during an fMRI session is associated with greater self-reported distress during daily social interactions.

The authors discuss that brain regions involved in processing social rejection-related information are most likely associated with a variety of biological responses to social and physical threat. Thus, these brain regions may have important implications for health and/or the individual’s susceptibility to inflammatory diseases.

SOURCE:  Proc Natl Acad Sci USA 2010, 107:14817. Epub 2010 Aug 2

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