Anterior Hypothalamic Lesions Inhibit Antigen-Induced Airway Eosinophilia in Rats

Abstract

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.

Lesions in the Suprachiasmatic Nuclei Suppress Inflammatory Mediators in Sensitized Rats

“…Previous electrolytic lesioning studies have shown that the lesions of the anterior hypothalamic area (AHA) provide reliable protection against the lethal effect of anaphylaxis in non-human primates [36, 37]. We also found that the AHA lesions resulted in the suppression of the LAR as assessed by the antigen-induced airway eosinophilic infiltration in rats of allergic inflammation [38]. These findings are consistent with the results obtained in our study.…”

“…Second, as mentioned in the introduction, we did not measure the circadian rhythms of either the inflammatory mediators or pulmonary functions, so it remains unclear whether the SCN plays a substantial part in the circadian rhythms of asthmatic responses. We could not completely rule out the possibility that the SCN lesioning might have influenced only peripheral allergic responses, but not the circadian rhythms, because some studies, including a report by us, have demonstrated changes in immunological parameters after brain damage [36,37,38,39]. Third, whether the SCN lesioning itself influences airway inflammation is unknown, because we did not investigate it using unsensitized control groups.…”

Role of anterior hypothalamus on asthma

“…Eidelman's late asthmatic response model of Brown Norway (BN) rats (200-250 g) were used [4]. Grouping was as follows:…”

“…0531 There are some reports that anterior hypothalamic lesion decreased the lethal anaphylaxis and suppressed the circulatory antibody and lymphocyte response to phytohemaggulutinin (PHA) mitogen in rats [1][2][3]. We reported previously the effect of anterior hypothalamic lesion using electrolytic method on late asthmatic response [4].…”