Because the prevalence of allergic diseases has significantly increased in recent years, understanding the causes and mechanisms of these disorders is of high importance, and intense investigations are ongoing. Current knowledge pinpoints immune tolerance mechanisms as indispensable for healthy immune response to allergens in daily life. It is evident that development and maintenance of allergens-pecific T cell tolerance is of vital importance for a healthy immune response to allergens. Such tolerance can be gained spontaneously by dose-dependent exposures to allergens in nature or by allergen-specific immunotherapy. Allergen-specific immunotherapy induces regulatory T cells with the capacity to secrete interleukin-10 and transforming growth factor-beta, limits activation of effector cells of allergic inflammation (such as mast cells and basophils), and switches antibody isotype from IgE to the noninflammatory type IgG4. Although allergen-specific immunotherapy is the only method of tolerance induction in allergic individuals, several factors, such as long duration of treatment, compliance problems, and life-threatening side effects, have limited widespread applicability of this immunomodulatory treatment. To overcome these limitations, current research focuses on the introduction of allergens in more efficient and safer ways. Defining the endotypes and phenotypes of allergic diseases might provide the ability to select ideal patients, and novel biomarkers might ensure new custom-tailored therapy modalities.
Allergens* ; Biomarkers ; Child* ; Compliance ; Humans ; Hypersensitivity ; Immune Tolerance* ; Immunoglobulin E ; Immunoglobulin G ; Immunotherapy ; Inflammation ; Interleukin-10 ; Mast Cells ; Phenotype ; Prevalence ; T-Lymphocytes, Regulatory

The aim of this study was to evaluate the synergistic potentiation effect of ineffective doses of dexmedetomidine on antinociception induced by morphine and fentanyl in acute pain model in rats. Seventy albino Wistar rats were separated into 7 groups. Data for the control and sham groups were recorded. The ineffective dose of dexmedetomidine was investigated and found to be 3 micro g/kg. Each group was administered the following medications: 3 mg/kg morphine (intraperitoneal) to Group 3, 5 microg/kg fentanyl (intraperitoneal) to Group 4, dexmedetomidine 3 micro g/kg (subcutaneously) to Group 5, dexmedetomidine 3 microg/kg (subcutaneous)+3 mg/kg morphine (intraperitoneal) to Group 6 and finally 3 microg/kg dexmedetomidine (subcutaneous)+5 microg/kg fentanyl (intraperitoneal) to Group 7. Just before the application and 15, 30, 60, 90 and 120 min after the administration of medication, two measurements of tail flick (TF) and hot plate (HP) tests were performed. The averages of the measurements were recorded. TF and HP latencies were the main outcomes. The analgesic effect of the combinations with dexmedetomidine+morphine (Group 6) and dexmedetomidine+fentanyl (Group 7), compared to the analgesic effect of morphine alone and fentanyl alone was significantly higher at 15, 30, 60 and 90 minutes after administration. In this study, dexmedetomidine in ineffective doses, when combined with morphine and fentanyl, potentiates the effects of both morphine and fentanyl.
Acute Pain* ; Animals ; Dexmedetomidine* ; Fentanyl* ; Morphine* ; Rats ; Rats, Wistar