Catecholamines mediate stress-induced increases in peripheral and central inflammatory cytokines

Area of Science:

• Neuroscience
• Immunology
• Pharmacology

Background:

• Proinflammatory cytokines are implicated in stress responses within the central nervous system (CNS).
• The precise mechanisms by which stress elevates peripheral and central proinflammatory cytokines remain unclear.
• Catecholamines are investigated for their potential role in mediating stress-induced cytokine induction.

Purpose of the Study:

• To investigate the role of catecholamines in the in vivo induction of proinflammatory cytokines following tailshock stress in rats.
• To elucidate the specific adrenoceptor subtypes involved in stress-induced cytokine responses.

Main Methods:

• Rats were pretreated with alpha1- (prazosin), beta- (propranolol), or combined alpha1/beta- (labetalol) adrenoceptor antagonists prior to tailshock stress.
• Plasma and tissue (hypothalamus, hippocampus, pituitary) levels of interleukin-1beta (IL-1beta) and IL-6 were measured post-stress.
• The effects of a neurotoxin targeting locus coeruleus projections and a beta-adrenoceptor agonist (isoproterenol) were also examined.

Main Results:

• Prazosin (alpha1 antagonist) reduced plasma IL-1beta and IL-6, but not tissue IL-1beta.
• Propranolol (beta antagonist) reduced plasma IL-6 and blocked tissue IL-1beta elevation.
• Labetalol reduced plasma IL-1beta and IL-6 and blocked pituitary IL-1beta, but not central tissue IL-1beta. Neurotoxin administration prevented hippocampal IL-1beta elevation.
• Isoproterenol induced circulating IL-1 and IL-6, and tissue IL-1beta.

Conclusions:

• Catecholamines are significantly involved in the induction of stress-induced proinflammatory cytokines.
• Beta-adrenoceptors are crucial for the induction of tissue IL-1beta.
• Both alpha- and beta-adrenoceptors contribute to the induction of plasma cytokines during stress.