Peripheral catecholamines are involved in the neuroendocrine and immune effects of LPS.

There is evidence for bidirectional communication between the brain and the immune system. The immune system is subjected to neuroendocrine influences and reciprocally the hypothalamopituitary-adrenal axis is modulated by immune signals. Lipopolysaccharides (LPS), used to mimic infectious/inflammatory diseases, induce a series of stress markers, including modifications of monoaminergic transmission, enhancement of HPA axis activity, and decreased immune activity. In the present work we investigated the participation of peripheral catecholamines in the immune and endocrine responses to LPS in vivo. We studied the effects of LPS after chemical sympathectomy using 6-hydroxydopamine (6-OHDA), which does not cross the brain-blood barrier (BBB) in adults when peripherally injected. 6-OHDA administration was able to interfere with the effects of LPS on immune cells; however, the effects depended on the lymphoid tissue tested. In fact, the depression of mitogenesis induced by LPS was reversed by 6-OHDA in the spleen but not in the thymus. Moreover, 6-OHDA also interfered with the endocrine modifications induced by LPS. This neurotoxin completely or partially inhibited the effect of LPS on ACTH and corticosterone secretion, respectively. Taken together, these results clearly demonstrate that in vivo, the peripheral sympathetic nervous system participates in the immune and endocrine effects of LPS.

No change in plasma corticosterone and splenic norepinephrine during humoral and cellular immune responses to sheep erythrocytes in C3H mice.

Host responses to immune stimulation, including antigenic stimulation and inflammation, have been described to involve the central neurotransmission, the hypothalamic-pituitary adrenal (HPA) axis, and the immune system. After antigenic stimulation, it has been hypothesized that the HPA axis is involved in a feedback mechanism which limits lymphocyte expansion linked to the immune response. However, such a stimulation of the HPA axis after immunization is not consistently reported in the literature. In the present experiments, we looked for a possible activation of the HPA axis, as well as for the involvement of the sympathetic nervous system during primary and secondary antibody synthesis and cellular immunity. C3H female mice were immunized with low or high doses of sheep red blood cells which induced delayed-type hypersensitivity (DTH) or antibody synthesis, respectively. Plasma corticosterone levels remained in normal ranges whether the animals developed primary or secondary humoral response or DTH. Splenic norepinephrine (NE) levels were unchanged during cellular immunity. During primary and secondary antibody responses splenic NE levels decreased, but no difference appeared between immunized animals and controls when the splenic NE content was expressed in milligrams per spleen because of a spleen enlargement in immunized animals. From these results, it can be concluded that immune responses, antibody synthesis and cellular immunity, in opposition to inflammation, may be induced without any detectable stimulation of the HPA axis or modification of the NE input in the spleen.(ABSTRACT TRUNCATED AT 250 WORDS)