Role of immune deviation by toll-liked receptor's doping LPS in pathogenesis of allergic rhinitis

Abstract

To investigate the role of TLR-NF-κB signaling pathway in pathogenesis of allergic rhinitis (AR) and the mechanism of TLR to modulate innate immunity and adaptive immunity. One hundred rats were divided into 5 groups by simple randomization, normal group(group A), modle group(group B), AR+LPS20 group(group C), AR+LPS10 group(group D), AR+LPS5 group(group E). Model of AR in B group was established by intraperitoneal injection and nasal topic delivery of ovalbumin (OVA). A group was delivered of same volume physiological saline instated of OVA, C,D,E group were interfered by nasal delivery of LPS in different concentration (including LPS 20 µg, 10 µg, 5 µg per 100 µl). Changes of nasal mucosa tissues and inflammatory cell infiltration were observed by HE staining, while neutrophil and eosinophil counted under high power microscope.Expression of IL-4, IFN-γ, and IgE in nasal mucosa tissues were measured with immunohistochemical method.Realtime-PCR and Western-blot were used to evaluate the expression level of TLR-4 and NF-κB in nasal mucosa tissues.SPSS 13.0 software was used to analyze the data. Group B was observed to have developed AR injury of nasal mucosa. Eosinophil count and the expression of IL-4, IFN-γ, and IgE were significantly higher in B group than those in A group (all P < 0.05), neutrophil count was significantly higher in C, D, E groups than that in B group (all P < 0.05). of immunohistochemical staining showed that, expression level of IFN-γ, TLR-4 and NF-κB were significantly higher than group B (all P < 0.05), while IL-4 and IgE were significantly decreased than group B (all P < 0.05) . The protein expression of TLR-4 and NF-κB was 0.888 9 ± 0.032 9 and 0.913 3 ± 0.031 1 in group C, and 0.419 2 ± 0.038 0 and 0.447 8 ± 0.033 0 in group A, 0.616 1 ± 0.025 1 and 0.748 1 ± 0.034 3 in group B, the difference was significant(all P < 0.05). TLR plays an important role of modulation between innate immunity and adaptive immunity in the pathogenesis of AR. The higher concentration of TLR doping may activate the higher expression of NF-κB then intervene the development of AR with immune deviation.