Stress decreases, while central nucleus amygdala lesions increase, IL-8 and MIP-1α gene expression during tissue healing in non-human primates

Ned H. Kalin, Steven E. Shelton, Christopher Gerald Engeland, H. Magnus Haraldsson, Phillip T. Marucha

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

Stress impairs healing and in part this effect is thought to be mediated by glucocorticoids. However, the brain systems that underlie the effects of stress on healing remain to be determined. Since the central nucleus of the amygdala (CeA) plays a role in mediating an individual's behavioral and physiological reactivity to stress, we investigated, in rhesus monkeys, whether selective lesions of the CeA altered the gene expression of chemokines (IL-8 and MIP-1α) that are associated with early dermal healing. We used rhesus monkeys because they provide an excellent animal model to investigate brain mechanisms relevant to human stress, anxiety, and psychopathology. Hypothalamic-pituitary-adrenal (HPA) activity was assessed in the monkeys prior to the wound healing experiment demonstrating that the CeA lesions reduce HPA activity. In the healing experiment, stress decreased IL-8 and MIP-1α gene expression in both CeA lesioned and non-lesioned animals. Conversely, the CeA lesions increased the tissue expression of IL-8 and MIP-1α mRNA prior to and after stress exposure. These results demonstrate that in primates the CeA is a key brain region involved in the regulation of processes associated with wound healing. Because of brain and behavioral similarities between rhesus monkeys and humans, these results are particularly relevant to understanding brain mechanisms that influence healing in humans.

Original languageEnglish (US)
Pages (from-to)564-568
Number of pages5
JournalBrain, Behavior, and Immunity
Volume20
Issue number6
DOIs
StatePublished - Nov 1 2006

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Interleukin-8
Primates
Gene Expression
Macaca mulatta
Brain
Wound Healing
Physiological Stress
Psychopathology
Chemokines
Glucocorticoids
Haplorhini
Central Amygdaloid Nucleus
Anxiety
Animal Models
Messenger RNA
Skin

All Science Journal Classification (ASJC) codes

  • Immunology
  • Endocrine and Autonomic Systems
  • Behavioral Neuroscience

Cite this

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title = "Stress decreases, while central nucleus amygdala lesions increase, IL-8 and MIP-1α gene expression during tissue healing in non-human primates",
abstract = "Stress impairs healing and in part this effect is thought to be mediated by glucocorticoids. However, the brain systems that underlie the effects of stress on healing remain to be determined. Since the central nucleus of the amygdala (CeA) plays a role in mediating an individual's behavioral and physiological reactivity to stress, we investigated, in rhesus monkeys, whether selective lesions of the CeA altered the gene expression of chemokines (IL-8 and MIP-1α) that are associated with early dermal healing. We used rhesus monkeys because they provide an excellent animal model to investigate brain mechanisms relevant to human stress, anxiety, and psychopathology. Hypothalamic-pituitary-adrenal (HPA) activity was assessed in the monkeys prior to the wound healing experiment demonstrating that the CeA lesions reduce HPA activity. In the healing experiment, stress decreased IL-8 and MIP-1α gene expression in both CeA lesioned and non-lesioned animals. Conversely, the CeA lesions increased the tissue expression of IL-8 and MIP-1α mRNA prior to and after stress exposure. These results demonstrate that in primates the CeA is a key brain region involved in the regulation of processes associated with wound healing. Because of brain and behavioral similarities between rhesus monkeys and humans, these results are particularly relevant to understanding brain mechanisms that influence healing in humans.",
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Stress decreases, while central nucleus amygdala lesions increase, IL-8 and MIP-1α gene expression during tissue healing in non-human primates. / Kalin, Ned H.; Shelton, Steven E.; Engeland, Christopher Gerald; Haraldsson, H. Magnus; Marucha, Phillip T.

In: Brain, Behavior, and Immunity, Vol. 20, No. 6, 01.11.2006, p. 564-568.

Research output: Contribution to journalArticle

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