Inhibition of TLR4 and NLRP3 leads to the exacerbation of IgE specific antibodies in mouse allergic models based on subcutaneous or intranasal immunization respectively
A significant increase in the prevalence of diseases linked with IgE production can be seen in recent years, but the question about the role of TLR receptors in this process remains controversial. According to the hygiene hypothesis, the decrease of the contact of the individual with pathogens that contain PRR receptor ligands in the recent years leads to the development of allergic diseases. The aim of this work was to investigate whether TLR4 and NLRP3 receptor activation contributes to allergen-specific antibody formation.BALB/c mice were immunized according to two different protocols. In the first one, OVA antigen was administered in 0.1 µg dose 2-3 times a week for 6 weeks by subcutaneous route. In the second one, OVA was administered in 0.3 µg dose intranasally in combination with 4 ng of benzo(a)pyrene (BaP) 2 times a week for 8 weeks. In both cases, TLR4 and NLRP3 receptor inhibitors, namely TLR4-IN-C34 in 1 mg/kg dose and CY- 09 in 20 mg/kg dose respectively were also administered to the some of the mice. Specific antibody production was determined by ELISA.Immunization of mice with TLR4-IN-C34 significantly (p