title: Role of adrenocorticotropic hormone in the modulation of pollinosis induced by pollen antigens.
abstract: BACKGROUND
  A mild restraint stressor suppressed an increase in the levels of Th2-dependent cytokines and IgE, thereby reducing the symptoms of pollinosis. In the present study, to clarify the mechanism of action of adrenocorticotropic hormone (ACTH) in improving the symptoms of pollinosis, we studied the effects of ACTH on the plasma level of histamine, mast cell number in nasal-associated lymphoid tissue (NALT) and the T cell differentiation in splenocytes.
  
  
  METHODS
  The role of ACTH in the development of pollen antigen-induced pollinosis was studied in mice. Allergic symptoms and parameters were measured on day 17 after sensitization. To investigate the effects of ACTH on T cell differentiation, we stimulated splenocytes obtained from control mice with ACTH and CD3/CD28 in vitro, and measured the cytokine production in the culture supernatant.
  
  
  RESULTS
  The plasma levels of IL-10, IgE and histamine and mast cell number in NALT were increased in the sensitized animals in association with a concomitant increase in the incidence of sneezing and nasal rubbing. The intraperitoneal administration of ACTH decreased the IL-10, IgE and histamine levels in the plasma and mast cell number in NALT, while increasing the IFN-γ level and suppressing the incidence of nasal rubbing. Furthermore, the production of IFN-γ increased, while the IL-4 level was suppressed after 2 days in culture.
  
  
  CONCLUSIONS
  The present findings showed that ACTH directly affects T cell differentiation and promotes Th1-type reactions. The regulation of the Th1/Th2 balance by ACTH may result in a decrease in the pathological features of pollinosis.
authors.affiliation: Department of Physiology, Osaka City University Medical School, Suzuka, Japan.
authors.forename: Maki
authors.initials: M
authors.lastname: Hashimoto
authors.forename: Eisuke F
authors.initials: EF
authors.lastname: Sato
authors.forename: Keiichi
authors.initials: K
authors.lastname: Hiramoto
authors.forename: Emiko
authors.initials: E
authors.lastname: Kasahara
authors.forename: Masayasu
authors.initials: M
authors.lastname: Inoue
authors.forename: Seiichi
authors.initials: S
authors.lastname: Kitagawa
mesh_terms: D000324:Adrenocorticotropic Hormone / Q000008:administration & dosage / Q000378:metabolism*; D000818:Animals; D052179:Antigens, Plant; D002454:Cell Differentiation / Q000276:immunology; D004195:Disease Models, Animal; D006632:Histamine / Q000097:blood*; D007073:Immunoglobulin E / Q000097:blood*; D007371:Interferon-gamma / Q000276:immunology*; D016753:Interleukin-10 / Q000097:blood*; D015847:Interleukin-4 / Q000276:immunology; D008407:Mast Cells / Q000276:immunology*; D051379:Mice; D008810:Mice, Inbred C57BL; D011058:Pollen / Q000276:immunology; D006255:Rhinitis, Allergic, Seasonal / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology*
chemical_list: D052179:Antigens, Plant; D016753:Interleukin-10; D015847:Interleukin-4; D007073:Immunoglobulin E; D006632:Histamine; D007371:Interferon-gamma; D000324:Adrenocorticotropic Hormone