ABSTRACT
OBJECTIVE: The excreted-secreted antigens (ESA) from the tachyzoites seem to play a key role in immunity against Toxoplasma gondii. The aim of this study is to investigate whether Alum-NLT mixture, as a new adjuvant, can induce humoral immunity in response to excreted secreted antigens (ESA) of Toxoplasma gondii as a model vaccine or not. METHODS: Six- to eight-week-old female Balb/c mice were divided into five groups. Mice in the experimental groups received either ESA vaccine alone or in combination with the adjuvant Alum, NLT or Alum-NLT mixture; Mice in the negative control group received phosphate buffered saline (PBS). All mice were immunised, three times subcutaneously (s.c.) with a total volume of 150µl each with a 10-day interval. Ten days after the final immunisation, immune response to Toxoplasma gondii was assessed. RESULTS: Our results revealed that Alum-NLT mixture as an adjuvant during vaccination boosts the efficacy of the ESA vaccine by means of increasing Toxoplasma gondii-specific IgG, IgG2a production and the ratio of IgG2a/IgG1 (P-value < 0.05). The use of this adjuvant mixture improved the protective immunity against Toxoplasma gondii. CONCLUSION: Administration of the Alum-NLT mixture as an adjuvant in ESA vaccine enhances humoral immunity.
Subject(s)
Adjuvants, Immunologic , Alum Compounds , Antibodies, Protozoan/blood , Immunoglobulin G/blood , Naltrexone/immunology , Protozoan Vaccines/immunology , Toxoplasma/immunology , Animals , Antigens, Protozoan/administration & dosage , Antigens, Protozoan/immunology , Female , Immunity, Humoral , Immunoglobulin G/immunology , Mice , Mice, Inbred BALB C , Models, Animal , VaccinationABSTRACT
The purpose of the present study was to examine the role of estrogen and prolactin in determining the responsiveness of tuberoinfundibular dopaminergic (TIDA) neurons to kappa-opioid receptor blockade in female rats. TIDA neuronal activity was estimated by measuring either dopamine synthesis [accumulation of 3,4-dihydroxyphenylalanine (DOPA) 30 min after the administration of the decarboxylase inhibitor NSD-1015] or metabolism [concentrations of 3,4-dihydroxyphenylacetic acid (DOPAC)] in terminals of these neurons in the median eminence. Blockade of kappa-opioid receptors with the selective kappa-antagonist norbinaltorphimine (NOR-BNI) increased the concentrations of DOPAC in the median eminence of ovariectomized rats but had no effect in gonadally intact rats, suggesting that loss of endogenous ovarian hormones following ovariectomy results in an increase in kappa-opioid-receptor-mediated inhibition of TIDA neurons. Estrogen administration ot ovariectomized rats blocked NOR-BNI-induced increases in median eminence DOPAC concentrations, whereas treatment of gonadally intact or ovariectomized, estrogen-treated rats with prolactin antiserum had no effect on the insensitivity of these neurons to NOR-BNI. Administration of antiserum to dynorphin A1-8 increased DOPA accumulation in the median eminence of ovariectomized but not estrogen-treated ovariectomized rats. Taken together, these results reveal that estrogen, acting via a prolactin-independent mechanism, suppresses kappa-opioid-receptor-mediated inhibition of the activity of TIDA neurons, possibly by decreasing the release of endogenous dynorphin.
Subject(s)
Brain Chemistry/drug effects , Dopamine/physiology , Estrogens/pharmacology , Median Eminence/metabolism , Neurons/physiology , Prolactin/physiology , Receptors, Opioid, kappa/drug effects , 3,4-Dihydroxyphenylacetic Acid/metabolism , Animals , Aromatic Amino Acid Decarboxylase Inhibitors , Dopamine/biosynthesis , Dynorphins/pharmacology , Female , Hydrazines/pharmacology , Hypothalamic Hormones/pharmacology , Injections, Intraventricular , Median Eminence/cytology , Median Eminence/drug effects , Naltrexone/analogs & derivatives , Naltrexone/immunology , Naltrexone/pharmacology , Nerve Endings/drug effects , Nerve Endings/metabolism , Neurons/drug effects , Ovariectomy , Peptide Fragments/pharmacology , RatsABSTRACT
A stereotactic electrolytic lesion of the anterior hypothalamic area in mice produces a rapid involution of the thymus and a reduction of lymphocytes in the peripheral blood. This effect on the thymus and blood lymphoid compartment can be prevented by postoperational administration of thyrotropin-releasing hormone (TRH) or melatonin. These activities of TRH or melatonin are antagonized by the opioid receptor blocker naltrexone. They do not seem to depend on stimulation of the thyroid gland or of the endogenous opioid system but rather on a direct activity of TRH on thymic targets or binding sites on lymphocytes.
