11 research outputs found
No change in plasma corticosterone and splenic norepinephrine during humoral and cellular immune responses to sheep erythrocytes in C3H mice
International audienc
Peripheral catecholamines are involved in the neuroendocrine and immune effects of LPS
International audienc
Sympathectomy-Induced Immune Changes Are Not Abrogated by the Glucocorticoid Receptor Blocker RU-486
Re-exposure to endotoxin induces differential cytokine gene expression in the rat hypothalamus and spleen
This study was designed to investigate whether the pattern of hypothalamic and splenic cytokine expression induced by peripheral administration of a bacterial lipopolysaccharide (LPS) is affected by prior exposure to LPS derived from another bacterial strain. Injection of LPS from Salmonella enteritidis (LPS2) alone resulted in increased hypothalamic gene expression of IL-1β, IL-6, TNFα, IL-1ra and IL-10. However, pre-exposure to LPS derived from Escherichia coli (LPS1) 3 weeks before, significantly attenuated hypothalamic IL-1ra, IL-6 and IL-10 expression. IL-1β expression also tended to be lower. This pattern contrasted with the robust cytokine expression in the spleen of LPS2-treated rats previously exposed to LPS1, since pre-treatment with endotoxin resulted in a significantly greater response of IL-1β and IL-1ra to LPS2. Expression of TNFα and IL-10 also tended to be higher. Pre-treatment with LPS1 did not significantly affect the marked increase in corticosterone and adrenaline blood levels induced by LPS2. Thus, while endotoxin pre-exposure seemed not to induce a “tolerant” state in the periphery as judged by the immune and endocrine parameters evaluated upon re-stimulation, expression of four of the six cytokines measured was decreased in the hypothalamus. This is the first demonstration that endotoxin priming can differentially affect cytokine expression in the central nervous system and peripheral tissues when a host is confronted with a second, acute, pro-inflammatory stimulus. These results may provide new evidence for the involvement of cytokine pathways in the central nervous system in modulating peripheral inflammation and mediating cognitive and behavioural alterations during inflammatory diseases