Abstract

Following exposure to the common cold (i.e., rhinovirus), locally produced nasal cytokines (rather than the infection itself) drive the progression of one’s symptoms (Hendley et al., 1973; Cohen et al., 1999). Stress-induced local inflammation exacerbates local cytokine production (e.g., marital hostility; Kiecolt-Glaser et al., 2005). An individual’s ability to effectively manage their emotions is a critical component of positive health and well-being. Here, we evaluated whether one’s self-reported frequency of cognitive reappraisal, an adaptive emotion regulation strategy, predicts nasal cytokine production following experimental rhinovirus exposure. Emotion regulation strategies were assessed at baseline prior to experimental infection. After the baseline assessment, each participant was exposed to a strain of rhinovirus (RV-39) and followed for 5 days in quarantine. Nasal interleukin (IL)-1β, IL-6, and IL-8 and subjective symptoms were assessed at baseline and on each of the 5 days of quarantine. A multilevel analysis of the data for 159 participants with documented infection demonstrated that less frequent use of cognitive reappraisal predicted heightened production of the nasal cytokine composite. Those who self-reported using cognitive reappraisal strategies less frequently displayed elevated nasal IL-6 and IL-8. Among the 63 participants with clinical cold, less frequent use of cognitive reappraisal was associated with heightened production of nasal IL-1β, IL-6, and IL-8. In ancillary analyses, the composite of nasal cytokines was associated with the severity of one’s subjective symptoms across the 5 days. Findings suggest that emotion regulation strategies, particularly cognitive reappraisal, influence illness trajectories during rhinovirus infection.

Highlights

  • Following exposure to the common cold, locally produced nasal cytokines drive the progression of one’s symptoms (Hendley et al, 1973; Cohen et al, 1999)

  • Local inflammation is responsible for the symptoms associated with the common cold; the present study aims to predict differences in biological mediators of illness expression based on one’s frequency of cognitive reappraisal

  • Those who selfreported using cognitive reappraisal strategies less frequently displayed elevated nasal IL-6 (b 1⁄4 À0.03, 95% CI [-0.06, À0.01], p 1⁄4 .016) and IL-8 (b 1⁄4 À0.03, 95% CI [-0.04, À0.01], p 1⁄4 .001) in response to the cold challenge. Those who self-reported using cognitive reappraisal strategies less frequently displayed somewhat elevated nasal IL-1β in response to the cold challenge, it was not statistically significant (b 1⁄4 À0.02, 95% CI [-0.04, À0.00], p 1⁄4 .061). Among those who met clinical criteria for the cold, less frequent use of cognitive reappraisal strategies was associated with significantly elevated nasal IL-1β (b 1⁄4 À0.07, 95% CI [-0.11, À0.03], p 1⁄4 .007), IL-6 (b 1⁄4 À0.07, 95% CI [-0.11, À0.03], p < .001), and IL-8 (b 1⁄4 À0.03, 95% CI [-0.06, 0.00], p 1⁄4 .042)

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Summary

The current study

Given the timing of when emotion regulation strategies occur, cognitive reappraisal might support control of affective responses during illness. Because cognitive reappraisal is associated with decreased systemic inflammation (Appleton et al, 2014), and psychosocial factors can impair local inflammatory processes (e.g., wound healing; Kiecolt-Glaser et al, 2005), we utilized data collected from the Pittsburgh Cold Study to investigate the influence of cognitive reappraisal on local inflammation among those infected and/or clinically ill from rhinovirus exposure. This question was novel, as local inflammation has not yet been investigated as a mechanism through which emotion regulatory strategies affect health outcomes. Our initial hypotheses are as follows: more frequent self-reported use of cognitive reappraisal will be associated with lower levels of nasal inflammation (as measured by a composite of IL-6, IL-8, and IL-1β) throughout the course of infection among both those infected (H1) and those with a clinical cold (H2)

Materials and methods
Statistical analysis
Fitting the model
10. Symptoms
Individual cytokines
Ancillary analyses
Discussion

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