A mosquito bite, a splinter, a virus infection, a bruise, or a broken bone will trigger an inflammatory response and dispatch cells and chemicals to the site to repair the damage.
Social stress can also induce inflammatory activity.
Stress-induced increases in inflammation have been implicated in several major disorders, including cardiovascular disease and depression but the neurocognitive pathways that underlie inflammatory responses to stress remain largely unknown.
George Slavich et al recruited 124 healthy young adult participants to complete a laboratory-based social stressor while markers of inflammatory activity were obtained from oral fluids.
As predicted, the laboratory-based social stressor tests showed that individuals who exhibit greater neural sensitivity to social rejection exhibit significant increases in two markers of inflammatory activity, namely a soluble receptor for tumor necrosis factor-α (sTNFαRII) and interleukin-6 (IL-6).
A subset of 31 participants later completed an MRI brain scan session in which their neural responses to social rejection were assessed.
Greater inflammatory activity was recorded in the dorsal anterior cingulate cortex and anterior insula. These are the brain regions that have previously been associated with processing rejection-related distress and negative affect.
These data elucidate a neurocognitive pathway that may be involved in potentiated inflammatory responses to acute social stress.
As such, they have implications for understanding how social stressors may promote susceptibility to diseases with an inflammatory component; these includes asthma, rheumatoid arthritis, cardiovascular disease, and depression.
Slavich GM, Way BM, Eisenberger NI, Taylor SE.Neural sensitivity to social rejection is associated with inflammatory responses to social stress. Proceedings of the National Academy of Sciences published ahead of print August 2, 2010Picture Credit