Depression of delayed-type hypersensitivity in mice with hypothalamic lesion induced by monosodium glutamate: involvement of neuroendocrine system in immunomodulation.
Delayed-type hypersensitivity (DTH) was depressed in mice that had been treated with monosodium glutamate (MSG) in their suckling period. Analysis of the DTH depression by use of the macrophage migration inhibition assay showed dysfunction of DTH effector T cells. The neuronal loss of nuclei in the hypothalamus, which elaborates the corticotropin-releasing factor and the hypersecretion of adrenocorticotrophic hormone, was observed in the MSG-treated mice. Therefore, DTH response may be modulated by the neuroendocrine system.
D000324:Adrenocorticotropic Hormone / Q000097:blood; D000818:Animals; D000942:Antigens, Bacterial / Q000276:immunology; D001500:BCG Vaccine / Q000276:immunology; D002464:Cell Migration Inhibition; D005260:Female; D006968:Hypersensitivity, Delayed / Q000276:immunology*; D007031:Hypothalamus / Q000276:immunology*; D007108:Immune Tolerance; D008089:Listeria monocytogenes / Q000276:immunology; D008264:Macrophages / Q000276:immunology; D008297:Male; D051379:Mice; D008809:Mice, Inbred C3H; D008815:Mice, Inbred Strains; D012970:Sodium Glutamate
D000942:Antigens, Bacterial; D001500:BCG Vaccine; D000324:Adrenocorticotropic Hormone; D012970:Sodium Glutamate