Electroacupuncture enhancement of natural killer cell activity suppressed by anterior hypothalamic lesions in rats.

BACKGROUND/OBJECTIVE: Neuroendocrine hormones are derived from the hypothalamus. The central nervous system, particularly the hypothalamus, is capable of modulating the cytolytic activity of adherent natural killer (NK) cells. In addition, electroacupuncture (EA) stimulation of the Zusanli (ST36) acupoint enhances splenic NK cell and cytokine activities in rats. However, it is still unclear whether the anterior hypothalamus affects this immunomodulation. Therefore, the aim of the present study was to examine the effect of EA stimulation at the Zusanli acupoint on the NK cell activity modulated by an anterior hypothalamic area lesion. METHODS: Male Sprague-Dawley rats were used. Lesions were placed by means of a direct current through a concentric electrode. The electric acupuncture stimulation was delivered for 30 min per each experiment at the right ST36 acupoint with an electrical stimulator. The NK cell activity of the spleen was measured by a fluorescence assay. RESULTS: The NK cell activity was significantly reduced on the 2nd day after the lesion, but was restored to that of the sham group by the 7th day. However, when EA was applied for 2 days after the operation, the NK cell activity of the lesion group was restored to that of the sham group. After 7 days of EA, the NK cell activity of the lesion group was slightly higher than that of the sham group. CONCLUSION: From these results, we can suggest that EA enhances or restores the NK cell activity suppressed by an anterior hypothalamic area lesion.

Anterior hypothalamic lesions inhibit antigen-induced airway eosinophilia in rats.

OBJECTIVE: Although previous studies have found that electrolytic lesions of the anterior hypothalamic area (AHA) resulted in the suppression of anaphylaxis, their effect on late allergic responses has scarcely been investigated. To clarify the role of the AHA on possible late asthmatic responses, including their neuroendocrinological mechanisms, we examined the effect of electrolytic AHA lesions on antigen-induced eosinophilic infiltration into the airway tract and measured the plasma corticosterone and catecholamine levels in sensitized rats, i.e. a model of bronchial asthma. METHODS: The rats were randomly divided into 3 groups, including: (1) an unoperated control group; (2) a sham AHA-lesioned group and (3) an AHA-lesioned group. Then, we investigated antigen-induced eosinophilic infiltration into right bronchoalveolar lavage fluid (BALF) and the lamina propria mucosae of the left main bronchus. RESULTS: The AHA-lesioned group showed the significantly lowest number of eosinophils in both the BALF (p < 0.01) and the main bronchus (p < 0.05). The plasma adrenaline levels in the AHA-lesioned group were significantly higher than those in the other groups (p < 0.05). No differences were found in the plasma corticosterone or noradrenaline levels among the 3 groups. CONCLUSION: This study provides evidence that AHA lesions inhibit not only anaphylaxis, but also late asthmatic response related to airway eosinophilic infiltration, possibly via an alteration of the sympathetic nervous function.

Plasma interleukin-1beta, prolactin, ACTH and corticosterone responses to endotoxin after damage of the anterior hypothalamic area.

This report concerns the use of an animal model described by us [J Submicrosc Cytol Pathol 1995;27:83-89] to investigate neural and endocrine sites for endotoxin (ENDO, E. coli 055:B5, 200 microg/100 g body weight in saline intravenously) effects on immunomodulatory hormone and cytokine release. Plasma interleukin-1beta (IL-1beta), prolactin (PRL), ACTH and corticosterone responses to ENDO after neurotoxic damage of neurons residing in the anterior hypothalamic area (AHA) were studied in freely behaving male rats. Excitotoxic cell damage in the AHA was produced by bilaterally injecting N-methyl-DL-aspartate (NMA) in artificial cerebrospinal fluid (aCSF) into this brain site. Injections of comparable volumes of aCSF alone served as controls for brain damage associated with the treatment. In both experimental brain manipulations before ENDO challenge the rise in plasma IL-1beta concentrations in response to ENDO was reduced by 2-fold at 1 h and 3- to 5-fold at 3 h when compared to controls. Nevertheless, experimental and control brain manipulations did not modulate the expected rise in corticosterone concentrations after ENDO exposure which rose 5-fold above the baseline level in all animals. However, AHA manipulation did reduce plasma ACTH and prolactin concentrations differentially. Introduction of either NMA or the control injection of aCSF alone into AHA reduced plasma ACTH concentrations by 2-fold at 0.5 and 1 h after ENDO. However, there was a greater reduction in the rise of plasma PRL concentrations after ENDO found in NMA-treated groups versus rats receiving control aCSF. These results demonstrate that variable-size hypothalamic damage (a larger lesion produced in AHA by NMA treatment vs. a smaller lesion control after aCSF) can result in a differential blunting of PRL, IL-1beta and ACTH release into blood in the face of robust, unmodulated corticosterone increases. In summary, these findings revealed a consistent predominant influence of ENDO on adrenal release of corticosterone as a concomitant to differential IL-1beta, ACTH and PRL release after AHA cell loss. In conclusion, these results constitute further evidence for hypothalamic orchestration of a balance between immunotropic and immunosuppressive neuroendocrine-immune events during acute bacterial infection of mammals.