The Role Of ER Stress In The Pathogenesis Of Allergic Rhinitis

Objective:To investigate the endoplasmic reticulum stress (ER-stress) related proteins differentially expressed in allergic rhinitis (AR) and normal control group turbinate tissue, endoplasmic reticulum stress mechanisms discussed in the pathogenesis of allergic rhinitis effect.Methods:To investigate to detect the endoplasmic reticulum stress associated marker GRP78, CHOP and "stress sensory" PERK, ATF6, XBP-1mRNA’s expression level in allergic rhinitis (AR) in inferior turbinate tissue viaquantitative real-time RT-PCR method; Toevaluatethe differences expression of GRP78in the two groups by immunohistochemical methods. Use the serial sections of immunohistochemical staining methods to detect GRP78protein expression and localization, and correlation to CD138expression cells and IgE; Utilizing common inflammatory factor to stimulate BEAS-2B cells to study the regulation of GRP78.Results:The result of real-time quantitative PCR showed GRP78, CHOP, PERK, XBP-1, ATF6’s mRNA expression level was significantly higher in the AR group and was statistically significant (PGRP78=0.021, PCHOP=0.001, PPERK=0.027, PXBP-1=0.025). mRNA expression level of GRP78and CHOP was almost a linear correlation (R=0.323, P=0.084, N=29). Stimulation factor dsRNA, LPS, IL-1β, IL-4, IFN-γ, IL-13, TSLP can up-regulation GRP78in BEAS-2B (PIL-1β=0.003, PIFN-γ=0.019, PIL-4=0.022, PIL-13=0.004, PdsRNA=0.03, PTSLP=0.006, PLPS=0.033). IL-4, IL-5, IL-10, IL-13, IL-17A, TLR2, TLR3, TRL4, TLR9, TSLP, IL-25, IL-1β’s mRNA expression level wew higher in AR than normal control (PIL-1β=0.001, PIL-4=0.029, PIL-5=0.002, PIL-13<0.001, PIL-17a=0.018, PTLR2<0.001, PTLR3=0.023, PTLR4=0.003, PTLR9=0.005, PTSLP<0.001, PIL-25=0.008, PLFN-8=0.001)。 In inferior turbinate tissue, GRP78expressed mainly in plasma cells (CD138) and ciliated columnar cells, and was linear correlated to CD138and IgE.. IL-5and IL-13were significantly higher in AR’s lavage.Conclusion:ER stress existedin AR; Upregulated cytokines in AR can induce the generation of ER stress; ER stress can promote the secretion of IgE, IL-5and IL-13in AR and thus involved in the pathogenesis of AR. Objective:To evaluate the relative factors influencing olfactory dysfunction in patients with chronic rhinosinusitis (CRS).Methods:Visual analogue scale (VAS) was applied to measure the severity of olfactory dysfunction of270patients with CRS. Patients were divided into two groups, one was that the quality of life (QoL) of patients was affected by olfactory dysfunction(VAS>5),the other was that without QoL affected by olfactory dysfunction (VAS≤5). The association between age, gender, nasal polyps, allergic rhinitis, smoking history, early nasal surgery history and other clinical factors, and serum total IgE level, peripheral blood eosinophil count, peripheral blood mononuclear cell count and olfactory dysfunction was analyzed.Results:The number ofpatients with nasal polyps, allergic rhinitis, previous nasal surgeries,the level of serum total IgE, and the severity of edema were significantly increased in patients with impaired QoL associated with olfactory dysfunction (P <0.05).,Serum total IgE increased (OR=1.003) and severe edema(OR=2.483) were the risk factors for the impairment of olfactory function, more notably for edema; whereas previous nasal surgerieswas a protective factor (OR=0.408). Sex distribution, age, smoking history, deviationofnasalseptum, eosinophil and mononuclear cell count did no statistically differ between the groups with and without impaired QoL associated with olfactory dysfunctions (P>0.05).Conclusion:Sever edema and increased serum total IgE are risk factors, whereas previous nasal surgeries history is a protective factor for the olfactory dysfunction.