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• W61422308 abstract "Abstract: It has been recognized for some time that the immune system can affect the central nervoussystemalteringbehavioralandneuroendocrineactivity.Thefocusoftheresearchhasbeenoncytokines,thehormones of the immune system, because cytokines are known to be secreted by immune cells when theyare activated, and administration of cytokines to animals can elicit many effects on the brain, specificallyneuroendocrine and behavioral effects. Cytokine administration also affects various neurotransmittersystems, which may underlie the neuroendocrine and behavioral effects. The most well‐studied effect isthe cytokine activation of the hypothalamo–pituitary–adrenocortical (HPA) axis. Interleukin‐1 (IL‐1)administered peripherally or centrally is a potent activator of the HPA axis. This property is shared bycertain other cytokines, IL‐2, IL‐6, tumor necrosis factor‐a (TNFa), and possibly the interferons (IFNs),although none is as potent or effective as IL‐1. Administration of IL‐1 also induces norepinephrine (NE)release in the brain, most markedly in the hypothalamus. Small changes in brain dopamine (DA) aresometimes observed, but these effects do not appear to be regionally selective. IL‐1 also increases brainconcentrations oftryptophan andthemetabolism ofserotonin(5‐HT)throughout thebraininaregionallynonselective manner. IL‐2 has similar but more modest effects on DA, NE, and 5‐HT. IL‐6 also increasestryptophan and5‐HTmetabolism, butdoes not affect NE. TNFa also activatesthe HPAaxis,but affects NEand tryptophan only at high doses. IFNa induces fever and HPA axis activation in man, but such effectshave not been confirmed in rodents. The reported effects of IFNs on brain catecholamines and serotoninhave been very inconsistent. However, interferon‐g has profound effects on the catabolism of tryptophan,converting it to kynurenine and quinolinic acid, effectively reducing its concentration in plasma. Thisaction may limit brain 5‐HTsynthesis by decreasing plasma tryptophan.Endotoxin (lipopolysaccharide, LPS) elicits HPA and neurochemical responses very similar to those ofIL‐1. Because LPS is known to stimulate the secretion of IL‐1, IL‐6, and TNFa, it is likely that these cytokinesmediateat least someoftheresponses. Bacterialand viral infectionsalso induceHPAactivation,and increasebrain tryptophan and brain NE and 5‐HTmetabolism. These effects are strikingly similar to those of IL‐1(asare the behavioral effects), suggesting that IL‐1 secretion, which accompanies many infections, may mediatethese responses. Studies with IL‐1 antagonists and using IL‐1‐knockout mice are consistent with thispossibility, although in most cases the antagonism is incomplete, suggesting the existence of multiplemechanisms. The neurochemical responses to cytokines are likely to underlie the physiological responses.TheNEresponsetoIL‐1appearstobeinstrumentalintheHPAactivation,butthisisnottheonlymechanismby which IL‐1 activates the HPA axis. Neither the noradrenergic nor the serotonergic systems appear to beinvolved in the major behavioral responses studied. The significance of the serotonin response is not known.ListofAbbreviations: COX,cyclooxygenase;CRF,corticotropin‐releasingfactor;CVOs,circumventricularorgans; DA, Dopamine; 5,7‐DHT, 5,7‐dihydroxytryptamine; DNAB, dorsal noradrenergic ascendingbundle; DOPAC, 3,4‐dihydroxyphenylacetic acid; GM‐CSF, Granulocyte/macrophage colony‐stimulatingfactor; 5‐HIAA, 5‐hydroxyindoleacetic acid; HPA, hypothalamo‐pituitary‐adrenocortical; 5‐HT,5‐hydroxytryptamine; HVA, homovanillic acid; IDO, indoleamine‐2,3‐dioxygenase; IFNs, Interferons;IL‐1, Interleukin‐1; IL‐1ra, IL‐1‐receptor antagonist; LPS, Lipopolysaccharide; MHPG, 3‐methoxy,4‐hydroxyphenylethyleneglycol; NDV, Newcastle disease virus; NE, Norepinephrine; NOS, nitric oxidesynthase; NTS, nucleus tractus solitarius; 6‐OHDA, 6‐hydroxydopamine; OVLT, organum vasculosumlaminae terminalis; PVN, paraventricular nucleus; SRBC, sheep red blood cells; TNFa, tumour necrosisfactor‐a; VNAB, ventral noradrenergic ascending bundle" @default.
• W61422308 created "2016-06-24" @default.
• W61422308 creator A5036520424 @default.
• W61422308 date "2008-01-01" @default.
• W61422308 modified "2023-09-26" @default.
• W61422308 title "3 Effects of the Immune System on Brain Neurochemistry" @default.
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