title: Salivary cytokine response in the aftermath of stress: An emotion regulation perspective.
abstract: Elevated inflammation in the context of stress has been implicated in mental and physical health. Approaching this from an emotion regulation perspective, we tested whether the salivary cytokine response to stress is dampened by using distraction to minimize opportunity for poststressor rumination. Healthy young adults were randomized to an acute stressor: modified Trier Social Stress Test (TSST, Study 1) or angry memory retrieval (Study 2). Within each study, participants were randomized to poststressor condition-rest or distraction-at a 3:1 ratio. Saliva, collected before and 40 min after the end of each stressor, was assayed for proinflammatory cytokines (PICs): interleukin-1β (IL-1β), TNF-α, and IL-6. Both stressors increased all PICs, and both provoked negative emotion. At 40 min post-TSST, salivary PIC increases did not differ between distraction and rest, but correlated positively with emotional reactivity to stress. At 40 min after memory retrieval, IL-1β increases and intrusive rumination were lower during distraction than rest, but did not correlate with emotional reactivity. Trait rumination and interference control mechanisms, also measured, played little role in PIC increases. Overall, after some stressors, some salivary cytokine responses are lower during distraction than rest. The roles of specific emotions, emotional intensity, and poststressor timing of saliva collection in this finding require clarification. Furthermore, the possibility of two affective paths to inflammation in the context of stress-one sensitive to opportunities for early occurring emotion regulation (as reflected in emotional reactivity), and one sensitive to late-occurring emotion regulation (as reflected in distraction after stress)-deserves attention. (PsycINFO Database Record
authors.affiliation: Department of Psychological and Brain Sciences, University of Louisville.
authors.forename: Tamara L
authors.initials: TL
authors.lastname: Newton
authors.affiliation: Department of Pathology and Laboratory Medicine, University of Louisville.
authors.forename: Rafael
authors.initials: R
authors.lastname: Fernandez-Botran
authors.affiliation: Department of Psychological and Brain Sciences, University of Louisville.
authors.forename: Keith B
authors.initials: KB
authors.lastname: Lyle
authors.affiliation: Department of Psychological and Brain Sciences, University of Louisville.
authors.forename: Yvette Z
authors.initials: YZ
authors.lastname: Szabo
authors.affiliation: Department of Pathology and Laboratory Medicine, University of Louisville.
authors.forename: James J
authors.initials: JJ
authors.lastname: Miller
authors.affiliation: Department of Psychological and Brain Sciences, University of Louisville.
authors.forename: Ashlee J
authors.initials: AJ
authors.lastname: Warnecke
mesh_terms: D000293:Adolescent; D000328:Adult; D001288:Attention / Q000502:physiology*; D016207:Cytokines / Q000032:analysis* / Q000378:metabolism*; D004644:Emotions / Q000502:physiology*; D005260:Female; D006801:Humans; D007249:Inflammation / Q000378:metabolism / Q000523:psychology; D053583:Interleukin-1beta / Q000032:analysis / Q000378:metabolism; D015850:Interleukin-6 / Q000032:analysis / Q000378:metabolism; D008297:Male; D000074222:Rumination, Cognitive / Q000502:physiology; D012463:Saliva / Q000737:chemistry* / Q000378:metabolism*; D013315:Stress, Psychological / Q000378:metabolism* / Q000523:psychology*; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis / Q000378:metabolism; D055815:Young Adult
chemical_list: D016207:Cytokines; D053583:Interleukin-1beta; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha