title: 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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Institute for Occupational Health Sciences, Aichi Medical University, Nagakute-cho, Aichi, Japan. irie@aichi-med-u.ac.jp
authors.forename: Masahiro
authors.initials: M
authors.lastname: Irie
authors.forename: Shoji
authors.initials: S
authors.lastname: Nagata
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Endo
mesh_terms: D000707:Anaphylaxis / Q000139:chemically induced / Q000276:immunology / Q000503:physiopathology; D000818:Animals; D007025:Anterior Hypothalamic Nucleus / Q000276:immunology* / Q000293:injuries / Q000503:physiopathology; D000941:Antigens / Q000276:immunology* / Q000494:pharmacology; D001249:Asthma / Q000276:immunology* / Q000503:physiopathology; D002395:Catecholamines / Q000097:blood; D003345:Corticosterone / Q000097:blood; D003714:Denervation; D004195:Disease Models, Animal; D008297:Male; D015213:Neuroimmunomodulation / Q000276:immunology*; D011657:Pulmonary Eosinophilia / Q000097:blood / Q000139:chemically induced / Q000276:immunology*; D051381:Rats; D013564:Sympathetic Nervous System / Q000276:immunology
chemical_list: D000941:Antigens; D002395:Catecholamines; D003345:Corticosterone