| Background and purposeAllergic rhinitis is one of the most common diseases in otolaryngology head and neck surgery.It is a type I allergic disease of nasal mucosa mediated by IgE,which affects people's quality of life and increases the social burden.According to statistics,the global average incidence rate is 10% ~ 25%,and with the development of global industrialization and the change of living environment,the incidence of allergic rhinitis rate has increased year by year in recent years,has become a global health problem to be solved.IgE is the most abundant immunoglobulin,mainly through the 2 cell receptor interactions play its pathological role,namely: high affinity Fc?RI and low affinity CD23(Fc?R?),have studied the interactions of molecular structure of IgE and Fc?RI and among the very mature and,as is the allergic disease of an important target.Recent studies on the structure of IgE receptors have shown that the binding sites of IgE and CD23 are more significant than those of Fc?RI,and CD23 may play a more important role in IgE mediated allergic diseases.A number of studies have shown that CD23 is involved in antigen Commission and transepithelial transport in the development of allergic airway and allergic enteritis.But also found in the study of allergic rhinitis,the expression of CD23 in nasal mucosa epithelial cells,one-way transport bidirectional transport and IgE antigen complexes involved in IgE induced degranulation of mast cells,and thus initiate allergic rhinitis.It is not clear whether CD23 mediates the occurrence of allergic rhinitis.Foreign studies have found that there is a CD23 dependent ERK signaling pathway in allergic enteritis,and the activation of ERK signaling pathway can further promote the release of CCL20 and IL8,which may lead to the development of inflammation.Whether there is the same CD23 mediated signaling pathway involved in the late inflammatory phase of allergic rhinitis in allergic rhinitis remains to be further explored.The research on the correlations and detected by CD23 and p-ERK,CCL20 and IL-18 expression in allergic rhinitis rat model,and blockade of CD23 in vivo,and observe its effects on the downstream ERK signaling pathway,so as to further understand the effects of CD23 on allergic rhinitis in the whole process,to further elucidate the pathogenesis of allergic rhinitis the search for new targets for the treatment of allergic rhinitis.Animals and methodsA rat model of allergic rhinitis was established.30 healthy SD rats were randomly divided into blank control group(A group),AR group(B group),CD23 group(n = C),each group had only 10 rats.A group and B C group,ovalbumin sensitized with ovalbumin and aluminum hydroxide base,with 5% ova saline solution nasal drops,1 times / day,for 10 days,C group in the ova saline solution intranasally challenged 30 minutes before giving anti-CD23 antibody intranasal treatment,1 times / day 10 consecutive days.Finally,the rats were exposed to nasal symptoms.HE staining was used to observe the histological changes of nasal mucosa and the expression of eosinophils.Immunofluorescence staining was used to detect the expression of CD23 and CCL20 in nasal mucosa of three groups,and the expression of p-ERK was detected by Western Blot.ELISA method was used to detect the levels of IgE,ECP,LTC4 and p-ERK,CCL20 and IL8 in serum of three groups of rats Result1.The levels of OVA-s IgE and LTC4 in the rats were significantly higher than those in the control group,while the CD23 antibody intervention group was significantly lower than the allergic rhinitis group,the difference between the three groups was statistically significant(P <0.05).2.The level of eosinophil infiltration and the level of ECP in the nasal mucosa of rats were significantly higher than those in the control group,while the CD23 antibody intervention group was significantly lower than the allergic rhinitis group,the difference between the three groups was statistically significant(P <0.05).3.The expression levels of CD23 in the nasal mucosa of the normal control group,AR group and CD23 antibody group were 51.32 ± 10.23,103.55 ± 19.98 and 72.63 ± 14.53 respectively,the difference was statistically significant(F = 78.41,P <0.05);4.The expression levels of p-ERK in the three groups were 79.37 ± 16.18,167.82 ± 31.42,117.43 ± 24.16 in the blank control group,the allergic rhinitis group and the CD23 antibody intervention group.The difference between the three groups was(F = 108.46,P <0.05).5.The expression of CCL20 in the blank control group,allergic rhinitis group and CD23 antibody intervention group was 40.82 ± 7.93,116.23 ± 23.17,63.47 ± 12.16,the difference between the three groups was statistically significant(F = 146.13,P <0.05).6.IL8 in the blank control group,allergic rhinitis group and CD23 antibody intervention group three groups of nasal lavage fluid expression was 18.32 ± 3.79,72.93 ± 15.21,31.26 ± 6.21,the difference between the three groups were statistically significant(F = 108.46,P <0.05).7.The expression of CD23 in the allergic rhinitis group was positively correlated with the level of p-ERK in the nasal cavity(P <0.05),and the expression of p-The level of ERK was also positively correlated with the levels of CCL20 and IL8(r = 0.792,r = 0.813 P <0.05).The level of IL8 in nasal lavage fluid was also positively correlated with eosinophils(r = 0.846,P <0.05)ConclusionCD23 not only mediate transport across the epithelial cells IgE and IgE immune complexes,start the occurrence of allergic rhinitis,also can activate ERK signal transduction pathway,CCL20,to promote the release of IL8,to recruit and chemotaxis of neutrophils,T lymphocytes and eosinophils in inflammatory induced local aggregation further amplification participate in the occurrence and development of allergic rhinitis in late phase.Therefore,the intervention of CD23 expression in nasal epithelial cells can be used as a new target for the treatment of allergic rhinitis. |
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