Cynical Hostility and Stimulated Th1 and Th2 Cytokine Production

Overview

Journal Brain Behav Immun

Publisher Elsevier

Specialties Allergy & Immunology
Neurology
Psychiatry

Date 2009 Aug 4

PMID 19647069

Citations 11

Authors

Denise Janicki-Deverts

Sheldon Cohen

William J Doyle

Affiliations

Soon will be listed here.

Abstract

Hostility has been associated with heightened proinflammatory activity. However, it is not known whether greater hostility contributes to greater inflammation by promoting higher Th1 activity, lower Th2 activity, or both. The present study examines the relation of hostility to mitogen-stimulated Th1 and Th2 cytokine production in vitro. Participants were 193 healthy men and women (mean age 37.3; 44% non-white). Hostility was assessed with a 20-item version of the Cook-Medley Hostility Scale (CMHS). PHA-stimulated interleukin (IL)-2, tumor necrosis factor (TNF)-alpha, and interferon (IFN)-gamma were used to measure Th1 activity; PHA-stimulated IL-4, IL-5, and IL-10 were used to measure Th2 activity. Greater hostility was related to greater production of two of the three Th1 cytokines, TNF-alpha and IFN-gamma. Hostility was not associated with any measure of Th2 cytokine production. Associations with Th1 cytokines were independent of age, sex, race, socioeconomic status, body mass index, depressive symptoms, and health-related behaviors, and were consistent across men and women. Associations were not explained by social network characteristics, social support, or personality traits closely associated with social behavior. Exploratory analyses substituting the CMHS cognitive, affective, and behavioral subscales for total hostility revealed that associations between hostility and Th1 cytokine production were primarily driven by the cognitive component of hostility (i.e., cynicism). Results suggest that a unique dimension of hostility, particularly the cynicism subcomponent, that is unrelated to social factors, may influence inflammation by promoting greater Th1 cytokine production. This effect on stimulated cytokine activity may have implications for a role of hostility in exacerbating immune-related disease.

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