scholarly journals Measuring local immunoglobulin E in the inferior turbinate nasal mucosa in patients with allergic rhinitis

2016 ◽  
Vol 65 (4) ◽  
pp. 396-399 ◽  
Author(s):  
Yasushi Ota ◽  
Yoshihiro Ikemiyagi ◽  
Toshiya Sato ◽  
Tatsuo Funakoshi ◽  
Nobuyuki Hiruta ◽  
...  
2014 ◽  
Vol 5 (1) ◽  
pp. ar.2014.5.0078 ◽  
Author(s):  
Seiichiro Makihara ◽  
Mitsuhiro Okano ◽  
Tazuko Fujiwara ◽  
Yohei Noda ◽  
Takaya Higaki ◽  
...  

Interleukin (IL)-17A is a major cytokine produced by Th17 cells, which are associated with chronic inflammations. The local expression of IL-17A in allergic rhinitis (AR) remains to be characterized. We sought to determine the role of IL-17A expression in human inferior turbinate mucosa in the pathophysiology of AR. Inferior turbinate mucosa was sampled from medical treatment-resistant, surgery-required patients with perennial AR (PAR, n = 21), nonallergic rhinitis with eosinophilia syndrome (NARES, n = 7), and nonallergic hypertrophic rhinitis (HR, n = 13). IL-17A expression was determined with immunohistochemical staining. The mean number of IL-17A+ cells and eosinophils per field were counted. Total serum immunoglobulin E (IgE) levels, blood eosinophil count, and forced expiratory volume in 1 second (FEV1)/forced vital capacity (FVC) ratio were also examined in each patient. IL-17A was primarily expressed in infiltrating inflammatory cells. The number of IL-17A+ cells in nasal mucosa was significantly higher in the PAR group compared with HR (p = 0.002) and NARES (p = 0.021) groups. There was a significant and positive correlation between the number of IL-17A+ cells and total nasal symptom score (rho = 0.403; p = 0.011), especially sneezing score (rho = 0.471; p = 0.003). The number of IL-17A+ cells was significantly and positively correlated with the degree of eosinophil infiltration (rho = 0.623; p < 0.001), but not with total serum IgE levels (rho = 0.284; p = 0.098), blood eosinophil counts (rho = 0.302; p = 0.056), or FEV1/FVC ratio (rho = 0.092; p = 0.569). The present study provides evidence that IL-17A expression in the nasal mucosa is associated with the pathophysiology of AR, including disease severity and nasal eosinophilia.


ORL ◽  
2021 ◽  
pp. 1-6
Author(s):  
Giancarlo Pecorari ◽  
Giuseppe Riva ◽  
Claudia Bartoli ◽  
Mattia Ravera ◽  
Valeria Dell’Era ◽  
...  

Introduction: Radiofrequency turbinate volume reduction (RFTVR) is an effective treatment of inferior turbinate hypertrophy. RFTVR can reduce epithelial cell alterations in nasal mucosa. The aim of this observational study was to evaluate the effects of RFTVR on nasal obstruction and cytology, stratifying for different types of rhinitis. Methods: Nasal cytology and subjective nasal obstruction were evaluated on 113 patients before RFTVR (T0) and after 3 months (T1). The patients were divided into groups on the basis of the underlying disease: allergic rhinitis, nonallergic rhinitis, rhinitis medicamentosa, and other diseases (e.g., hormonal-based turbinate hypertrophy). Results: Nasal cytology at T0 identified 42 patients with allergic rhinitis, 40 with nonallergic rhinitis, 19 with rhinitis medicamentosa, and 12 with other diseases. An improvement of nasal cytology at T1 was observed in 29.2% of cases. They mainly consisted of patients with nonallergic rhinitis with neutrophils, whose neutrophil infiltrate decreased. Only 2 cases (1.7%) showed a worsening of nasal cytology at T1. A statistically significant decrease in subjective nasal obstruction was observed for every group (p < 0.05). Higher differences of nasal obstruction between T0 and T1 were found in patients with rhinitis medicamentosa or other diseases. Conclusion: RFTVR represents a safe and effective treatment for turbinate hypertrophy of various etiology. It is not responsible for a worsening of inflammatory infiltrate of the nasal mucosa.


2014 ◽  
Vol 67 (suppl. 1) ◽  
pp. 49-56
Author(s):  
Maja Buljcik-Cupic ◽  
Dragana Lemez ◽  
Slobodan Savovic ◽  
Ljiljana Jovancevic ◽  
Danijela Dragicevic

Local allergic rhinitis is a localized allergic response of the nasal mucosa to aeroallergens in the absence of atopy with characteristic production of specific local immunoglobulin E antibodies in the nasal mucosa, T helper type 2 cellular infiltration response during the exposure to aeroallergens and positive results via the nasal allergic provocation test with the release of inflammatory mediators (triptase and eosinophil cationic proteins). Even though the prevalence of local allergic rhinitis has been and is still being investigated, a large number of patients with diagnosed non-allergic rhinitis or idiopathic rhinitis are currently classified as having local allergic rhinitis. The causes of local allergic rhinitis are most commonly house dust, dust mites, pollens and many others. Diagnosis of local allergic rhinitis is made using nasal allergen provocation tests when the prick test for standard inhalation allergens and the serum specific immunoglobulin analysis for aeroallergens are negative. The increasing amount of data on localized allergic response in non-atopic patients asks for many answers regarding local allergic rhinitis. These answers can be obtained by a study on the prevalence and incidence in children and adults, the impact of positive family atopy in the development of disease, the impact of associated diseases of the lower respiratory tract and conjunctiva, the effectiveness of drug treatment and the issue of administration of specific immunotherapy.


2021 ◽  
Vol 35 (6) ◽  
pp. 781-789
Author(s):  
Zhiqi Ma ◽  
Haijuan Lian ◽  
Xiaoyan Lin ◽  
Yong Li

Background Allergic rhinitis (AR) is one of the most common noninfectious respiratory diseases caused by immunoglobulin E (IgE) response. Objective The study sought to explore the relationship between lncRNA MIAT and miR-10b-5p and their interaction in the regulation of allergic phenotypes in allergic rhinitis (AR) mice. Methods A mice model of AR was constructed using ovalbumin (OVA) sensitization. AR mice were treated with miR-10b-5p agomiR and LNA mediated lncRNA MIAT. The targeting relationship between MIAT and miR-10b-5p was analyzed by the ENCORI website and dual-luciferase reporter assay. The numbers of rubbing and sneezing of mice were counted. Hematoxylin-eosin (HE) staining visualized the eosinophils infiltration in nasal mucosa tissues of mice. The percentage of Th17 cells was quantitated by flow cytometry analysis. ELISA was used to detect the levels of serum OVA-specific IgE, the Th12 cytokine IL-4, and inflammatory cytokines (IL-6, IL-17). Results MIAT was up-regulated in the nasal mucosa of AR mice, while miR-10b-5p was down-regulated. MIAT directly suppressed miR-10b-5p expression in AR mice. The numbers of rubbing and sneezing, the percentage of Th17 cells, and the levels of OVA-specific IgE, IL-4, IL-6, and IL-17 in AR mice were decreased by miR-10b-5p overexpression, which was reversed by MIAT overexpression. The eosinophils infiltration in AR mice was inhibited by miR-10b-5p overexpression, which was also reversed by MIAT overexpression. Conclusion The present study demonstrates that MIAT overexpression Promotes allergic inflammation and symptoms by activating Th17 immune response via miR-10b-5p inhibition.


2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Maria Lauriello ◽  
Alessandra Micera ◽  
Paola Muzi ◽  
Lino Di Rienzo Businco ◽  
Sergio Bonini

Background. Toll-like receptors (TLRs) represent a family of evolutionarily conserved proteins, that represent a fundamental link between innate and adaptive immune responses.Aim. The purpose of this study was to investigate the expression of TLR4 and TLR9 in the normal nasal mucosa and in the mucosa of subjects with different phenotypes of rhinitis.Methodology. A confocal analysis of TLR4 and TLR9 (co)expression was carried out on biopsies from the inferior turbinate obtained from 4 patients affected by persistent allergic rhinitis, 8 patients with chronic rhino-sinusitis, and 6 patients with vasomotor rhinitis The results were compared with those of specimens obtained from 4 subjects undergoing nasal surgery, but with signs of nasal inflammation.Results. TLR4 and TLR9 were expressed in the healthy nasal mucosa; TLR4 and TLR9 expression was significantly decreased in allergic rhinitis. TLR4 was over expressed in the epithelium of chronic rhino-sinusitis. Both TLRs were co-expressed in the sub-epithelial infiltrate of chronic and vasomotor rhinitis, even though this expression was higher in the former compared with the latter.Conclusions. This study indicates that TLR4 and TLR9 show a different pattern of expression in different phenotypes of rhinitis, possibly related to the type and severity of the disease.


2019 ◽  
Vol 33 (5) ◽  
pp. 524-530 ◽  
Author(s):  
Aneeza W. Hamizan ◽  
Mark Azer ◽  
Raquel Alvarado ◽  
Peter Earls ◽  
Henry P. Barham ◽  
...  

Background Not all rhinitis patients are affected by an immunoglobulin E (IgE)-mediated inflammatory process. Skin and serum allergy assessments are limited in their ability to define local allergic rhinitis (LAR). Thus, patients with negative systemic allergy assessments comprise a mix of those who truly have nonallergic rhinitis (NAR) and patients with LAR. Objective To determine the clinical characteristics of patients with NAR. Methods A cross-sectional study was performed on consecutive adults with rhinitis symptoms who underwent turbinate surgery. NAR patients were defined by excluding allergy using both systemic (serum-specific IgE and/or skin prick test) and local (inferior turbinate tissue-specific IgE) tests. Allergic rhinitis (AR) patients were defined by any positive systemic or local test toward aeroallergens. The clinical characteristics studied included allergic comorbidities (asthma, eczema, allergic conjunctivitis), inhalant allergen triggers (dust, pollen, animal dander), and environmental triggers (Cincinnati Irritant Index [CII]). Results There were 154 participants (41.79 ± 14.78 years, 37.7% female). NAR patients (11.7%) were older (49.33 ± 15.99 vs 40.78 ± 14.38 years, P = .02), had less self-reported asthma (5.6% vs 36.3%, P < .01) and house dust inhalant trigger (38.9 vs 65.2%, P = .03) compared to AR patients. The CII score was similar for NAR and AR (31.06 ± 28.88 vs 35.49 ± 24.70, P = .61). Conclusion Patients who were older, without asthma, and lacked an inhalant allergy trigger were more likely to have true NAR. Environmental triggers are not distinguishing features of NAR. This may be used as a guide to identify rhinitis patients whose symptoms are truly nonallergic etiology compared to those with falsely negative systemic allergy assessment but may still need management for LAR.


1996 ◽  
Vol 110 (10) ◽  
pp. 929-933 ◽  
Author(s):  
A. Slater ◽  
L. A. Smallman ◽  
A. B. Drake-Lee

AbstractThe aim of the study was to compare the numbers and distribution of mast cells in the nasal mucosa of perennial allergic rhinitis (PAR) patients and controls, as demonstrated by different staining methods for light microscopy.Biopsies of inferior turbinate mucosa were taken from 10 patients with PAR and 10 patients undergoing septoplasty or septorhinoplasty (control group). Sections for light microscopy were stained with azure A, chloroacetate esterase and an ABC immunohistochemical technique using antibody to tryptase.Three times more mast cells were found in the epithelium of PAR patients compared to controls using the immunohistochemical technique (p = 0.0074). This method demonstrated considerably more mast cells than the other stains.The increase in epithelial mast cells is consistent with the migration of mast cells seen in seasonal allergic rhinitis, and this may be important in the phenomenon of nasal priming seen after repeated antigen exposure.


2021 ◽  
Vol 17 (1) ◽  
Author(s):  
Jia Wang ◽  
Jinshu Yin ◽  
Hong Peng ◽  
Aizhu Liu

Abstract Background To investigate the role of microRNA-29 (miR-29) in mice with allergic rhinitis (AR) and its underlying mechanism. Methods AR model was established in BALB/c mice by intraperitoneal sensitization and intranasal challenge with ovalbumin (OVA). miRNA expression was examined in the nasal mucosa tissues of mice and patients with AR, and miRNA-29 was found to be downregulated. To unveil the role of miRNA-29 in AR, it was overexpressed in the nasal mucosa of AR mice by intranasal administration of miRNA-29 agomir. The symptoms of nasal rubbing and sneezing were recorded and evaluated. miR-29 expression, OVA-specific immunoglobulin E (IgE) concentration, pro-inflammatory cytokines levels, eosinophils number, and cleaved caspase-3 and CD276 expression were examined in nasal mucosa tissues and nasal lavage fluid (NALF) by qRT-PCR, ELISA, hematoxylin and eosin staining, western blotting, or immunohistochemistry, respectively. TUNEL assay was used to analyze nasal mucosa cells apoptosis. Results Decreased expression of miR-29 was observed in AR, the symptoms of which were alleviated by overexpressing miR-29. In addition, overexpression of miR-29 markedly reduced the concentration of OVA-specific IgE, the levels of IL-4, IL-6, IL-10, and IFN-γ, the pathological alterations and eosinophils infiltration in the nasal mucosa. Furthermore, restoration of miR-29 expression reduced nasal mucosa cell apoptosis. Moreover, overexpression of miR-29 significantly attenuated CD276 mRNA and protein levels in nasal mucosa cells. Conclusion MiR-29 mediated antiallergic effects in OVA-induced AR mice by decreasing inflammatory response, probably through targeting CD276. MiRNA-29 may serve as a potential novel therapeutic target for the treatment of AR.


Author(s):  
Mahita Bellamkonda ◽  
Vinod Kumar

ABSTRACTObjectives: Allergic rhinitis (AR) is on the rise in our society for various reasons. It is said that allergy might represent a primary or secondary factorin up to half the patients encountered in an otolaryngology practice. Thus, the management of AR constitutes a large proportion of the day-to-daypractice. In addition to its primary effect, inhalant allergy of the upper respiratory tract might affect the development and clinical course of otherdisease states such as sinusitis, otitis media, and asthma due to the mucosal continuity. Hence, this study was conducted to know the comorbidassociations of AR and also the pathology in inferior turbinate hypertrophy (ITH).Methods: A time-bound, descriptive cross-sectional study was conducted in ENT OPD. Patients were selected for the study after proper history taking,clinical examination, laboratory investigations such as absolute eosinophil count (AEC) and diagnostic nasal endoscopy, and consent for biopsy frominferior turbinate and histopathological examination using predefined inclusion and exclusion criteria. Nasal symptoms of sneezing, rhinorrhea, nasalpruritus, nasal obstruction, anosmia and non-nasal symptoms of eye itching, watering, foreign body sensation, and pharyngeal itching were recorded.Results: The mean age of the patients was 27.08 years with a standard deviation of 6.1. Patients were clinically evaluated regarding symptoms inear, nose, throat, eyes, and respiratory system. All patients had nasal symptoms whereas 53.34% patients had ophthalmic and pharyngeal symptoms.Aural comorbidity was most common with complaints in 68.33% followed by respiratory symptoms in 30% patients. About 40% patients complainedof sleep disturbances. Nearly 31.67% patients had a positive family history. The pale nasal mucosa was seen in 63.33% patients. Almost 70% patientshad intermittent AR, of which 43.33% had a mild degree. About 55% cases had AEC <350 cells/cumm. Almost 51.67% patients had more than fiveeosinophils per high power field in the biopsy of their inferior turbinates.Conclusion: Although most patients presented with nasal symptoms, ophthalmic and pharyngeal symptoms were commonly presented. ITH withpale nasal mucosa were the most common examination findings. Although AEC was not raised in most of the patients, more than half patients hada raised eosinophil count in the inferior turbinate biopsy. Thus, in a patient with AR, special attention has to be given to the ear, throat, eye, andasthmatic aspect. Eosinophil count in inferior turbinate biopsy is fairly reliable indicator in allergic turbinates.Keywords: Allegic rhinitis, Asthma, Absolute eosinophil count, Eosinophil count, Inferior turbinate biopsy.


2017 ◽  
Vol 42 (3) ◽  
pp. 901-912 ◽  
Author(s):  
Lifeng Xiao ◽  
Li Jiang ◽  
Qi Hu ◽  
Yuru Li

Background: Emerging evidences indicate that post-transcriptional regulation by microRNAs is critical in allergic rhinitis (AR) pathogenesis. MircroRNA-133b (miR-133b) was recently suggested as a potential predictor of AR. However, the in vivo effect of miR-133b on AR is unclear. Methods: AR model was established in BALB/c mice by intraperitoneal sensitization and intranasal challenge with ovalbumin (OVA). MiR-133b agomir was then intranasally administrated to mice after OVA challenge for another 7 days. The symptom of nasal rubbing and sneezing were recorded after the last OVA challenge. Nasal mucosa tissues and serum were collected. MiR-133b expression, serum OVA-specific immunoglobulin E (IgE) concentration, proinflammatory cytokines (TNF-α, IL-4, IL-5, IL-10 and IFN-γ) levels, and Nlrp3 inflammasome activation were measured by RT-PCR, ELISA, western blotting or immunohistochemistry, respectively. Histopathologic changes were evaluated using hematoxylin and eosin and Sirius red staining. The luciferase activity and protein expression of Nlrp3 were also determined. Results: MiR-133b expression was significantly decreased in nasal mucosa of AR mice, which was restored by nasal administration with miR-133b agomir. Upregulation of miR-133b markedly reduced the concentration of OVA-specific IgE, the frequencies of nasal rubbing and sneezing, and the levels of cytokines (TNF-α, IL-4, IL-5 and IFN-γ). Levels of IL-4, IL-5, IL-10 and IFN-γ produced by cervical lymph node cells were significantly lowered in miR-133b agomir-treated mice. Moreover, miR-133b also appeared to strongly attenuate pathological alterations and eosinophils and mast cells infiltration in nasal mucosa. Notably, we demonstrated for the first time that miR-133b negatively regulated Nlrp3 expression through binding with the 3’ untranslated region of Nlrp3. Consequently, infection of miR-133b in nasal mucosa remarkably suppressed the Nlrp3 inflammasome activation, as evidenced by reduced Nlrp3, Caspase-1, ASC, IL-18 and IL-1 expressions. Conclusion: MiR-133b alleviates allergic symptom in AR mice by inhibition of Nlrp3 inflammasome-meditated inflammation. These findings provide us an insight into the potential role of miR-133b in relation to AR treatment.


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