Social regulation of leukocyte homeostasis: the role of glucocorticoid sensitivity.

TitleSocial regulation of leukocyte homeostasis: the role of glucocorticoid sensitivity.
Publication TypeJournal Article
Year of Publication2008
AuthorsCole SW
JournalBrain Behav Immun
Date Published2008 Oct
KeywordsAged, Emotions, Female, Glucocorticoids, Homeostasis, Humans, Hypothalamo-Hypophyseal System, Interpersonal Relations, Leukocytes, Lymphocytes, Male, Middle Aged, Monocytes, Neutrophils, Pituitary-Adrenal System, Social Environment, Social Isolation, Statistics as Topic, Taiwan

Recent small-scale genomics analyses suggest that physiologic regulation of pro-inflammatory gene expression by endogenous glucocorticoids may be compromised in individuals who experience chronic social isolation. The present study assessed the relationship between leukocyte distributional sensitivity to glucocorticoid regulation and subjective social isolation in a large population-based sample of older adults. Initial analyses confirmed that circulating neutrophil percentages were elevated, and circulating lymphocyte and monocyte percentages were suppressed, in direct proportion to circulating cortisol levels. However, leukocyte distributional sensitivity to endogenous glucocorticoids was abrogated in individuals reporting either occasional or frequent experiences of subjective social isolation. This finding held in both non-parametric univariate analyses and in multivariate linear models controlling for a variety of biological, social, behavioral, and psychological confounders. The present results suggest that social factors may alter immune cell sensitivity to physiologic regulation by the hypothalamic-pituitary-adrenal axis in ways that could ultimately contribute to the increased physical health risks associated with social isolation.

Alternate JournalBrain Behav. Immun.
PubMed ID18394861
PubMed Central IDPMC3004947
Grant ListAG16661 / AG / NIA NIH HHS / United States
AG16790 / AG / NIA NIH HHS / United States
CA116778 / CA / NCI NIH HHS / United States
R01 CA116778 / CA / NCI NIH HHS / United States
R01 CA116778-03 / CA / NCI NIH HHS / United States