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Acute Stress Induces Proinflammatory Signaling at Chronic Inflammation Sites

From Institute of Medical Psychology (U.W.), Department of Periodontology (A.H.), Research Group Immunobiology (V.K.-B.), University of Duesseldorf, Duesseldorf, Germany; Institute of Medical Psychology (R.D.), University of Giessen, Giessen, Germany.

Address correspondence and reprint requests to Renate Deinzer, Institute of Medical Psychology, University of Giessen, Friedrichstrasse 36, 35392 Giessen, Germany. E-mail: renate.deinzer{at}psycho.med.uni-giessen.de

Objectives: To analyze in a randomized controlled study whether acute psychological stress alters local proinflammatory signals in a human model of chronic inflammation, i.e., gingivitis. Chronic inflammation represents a crucial factor in a variety of diseases and factors that contribute to the onset and progression of disease. Psychological stress is assumed to represent such a factor. However, experimental human research in this area is rare.

Methods: A total of 25 students (n = 11 females, 14 males) suffering from gingivitis were subjected to a stress (public-speaking task) and to a control condition in randomized order. Local concentrations of interleukin (IL)-8 were quantified as an indicator of proinflammatory activity at sites of inflammation. IL-8 is a strong proinflammatory mediator and involved in a variety of disease processes. Samples were taken at sites of inflammation before stress versus control condition and 0, 45, and 90 minutes afterward.

Results: A significant main effect (p = .03) of acute stress on local IL-8 was found. Stress induced an increase of IL-8-concentrations; univariate effect sizes varied between d = 0.23 and d = 0.36.

Conclusion: This is the first human experimental in vivo study demonstrating that psychological stress alters the local concentrations of IL-8 under conditions of chronic inflammation. It provides direct evidence acute stress is involved in the regulation of local proinflammatory responses in chronic inflammation. Future studies should now explore the effects of more enduring stress conditions and the factors mediating stress effects on inflammatory signals.

Key Words: stress • chronic • inflammation • proinflammatory response • interleukin-8

Abbreviations: IL = interleukin; GCF = gingival crevicular fluid; CRH = corticotrophin-releasing hormone; SP = substance P.