American Journal of Rhinology & Allergy最新文献

Background: Immune-related diseases can interact with each other, and growing evidence suggests that these diseases are associated with allergic rhinitis (AR). However, it is unclear whether previously observed associations reflect causal relationships.

Objective: This study estimated the genetic association between various immune-related diseases and AR using two-sample Mendelian randomization (MR).

Methods: Eight immune-related diseases were selected as exposure factors, and AR was selected as the outcome. The 8 immune-related disease categories included atopic dermatitis (AD), Graves' disease (GD), asthma, Crohn's disease (CD), multiple sclerosis (MS), rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and ulcerative colitis (UC). Data from GWAS (Genome-Wide Association Studies) were selected to construct instrumental variables (IVs) for each disease, and multiple single-nucleotide polymorphisms (SNPs) were selected as IVs. Corresponding data were retrieved according to the selected SNPs, and all data were summarized and analyzed.

Results: A total of 416 SNPs were screened as IVs, and the results of IVW support a causal relationship between AR risk and AD (OR: 1.026, 95% CI: 1.014-1.038, P = 9.59 × 10^-6), asthma (OR: 1.057, 95% CI: 1.029-1.086, P = .0001), and CD (OR: 1.006, 95% CI: 1.002-1.011, P = .0085). Furthermore, GD (OR: 0.995, 95% CI: 0.991-0.999, P = .0213) and SLE (OR: 0.997, 95% CI: 0.995-1.000, P = .025) may be protective factors.

Conclusion: This MR study found that AD, asthma and CD increase the risk of AR in populations of European ancestry, GD and SLE may be protective factors. These results suggest that confounding factors may have influenced associations previously reported in observational studies.

Background: Airway remodeling is demonstrated in Asian patients with allergic rhinitis (AR). The epithelial-mesenchymal transition (EMT) is one of the key mechanisms underlying airway remodeling. Thymic stromal lymphopoietin (TSLP) is an important contributor to airway remodeling. Although increased TSLP is found in AR, little is known about whether TSLP is involved in airway remodeling through induction of the EMT.

Objective: We investigated the effect of TSLP on the EMT in human nasal epithelial cells (HNECs) from AR patients.

Methods: Human nasal epithelial cells from AR patients were stimulated with TSLP in the absence or presence of the preincubation with a selective inhibitor of transforming growth factor beta 1 (TGF-β1) receptor (SB431542). The expression of TGF-β1 in the cells was evaluated by using real-time polymerase chain reaction, Western blotting, and immunocytochemistry. Western blotting and immunocytochemistry were used to assay EMT markers including vimentin, fibroblast-specific protein 1 (FSP1) and E-cadherin, small mothers against decapentaplegic homolog2/3 (Smad2/3), and phosphorylated Smad2/3 in the cells. The levels of extracellular matrix components such as collagens I and III in supernatants were measured by enzyme-linked immunoassay. Morphological changes of the cells were observed under inverted phase-contrast microscope.

Results: A concentration-dependent increase of TGF-β1 mRNA and protein was observed following stimulation with TSLP. Furthermore, TSLP decreased the expression of E-cadherin protein, but upregulated the production of FSP1 and vimentin proteins along with increased levels of collagens I and III, and the morphology of the cells was transformed into fibroblast-like shape. Additionally, a significant increase was found in phosphorylation of Smad2/3 protein. However, these effects were reversed by SB431542 preincubation.

Conclusion: TSLP-induced HNECs to undergo the EMT process via TGF-β1-mediated Smad2/3 activation. TSLP is an activator of the EMT in HNECs and might be a potential target for inhibiting EMT and reducing airway remodeling in AR.

Background: Evidence has shown that glucocorticoid-induced transcript 1 (GLCCI1) single nucleotide polymorphism (SNP) rs37937 is associated with asthma.

Objectives: The objective of this study was to investigate whether the GLCCI1 SNP rs37937 is a risk factor for allergic rhinitis (AR) in a Chinese Han population.

Methods: A total of 220 individuals including 109 AR patients and 111 healthy subjects were included. The genotyping of GLCCI1 rs37973 was performed by the SNaPshot method. The correlations of rs37973 polymorphism, AR risk, and clinical characteristics were further analyzed, as well as the treatment response to intranasal corticosteroids (INCS) in AR patients of different genotypes.

Results: Three GLCCI1 rs37973 SNP genotypes were identified in both AR patients and healthy subjects. Significant association between rs37973 polymorphism and AR under allele model, dominant model, heterozygote model, and homozygote model were shown. The A allele frequency of SNP rs37973 in AR was significantly higher than that in controls. The serum total immunoglobulin E (IgE) in AR patients of AA genotype was significantly higher than in patients of GA and GG genotype, and the serum total IgE in GA genotype was significantly higher than in GG genotype. Interestingly, after 4 weeks of INCS treatment for AR patients, the improvement of the nasal itching score, sneezing score, runny nose score, total nasal symptom score, and visual analog scale score of the GG genotype were worse than the AA or GA genotype.

Conclusion: The GLCCI1 rs37937 polymorphism is associated with the risk of developing AR and the response to INCS treatment in the Chinese Han population.

Background: Neurokinin-1 receptor (NK-1R) and normal T cell expressed and secreted (RANTES) have been shown to play important roles in allergic rhinitis (AR). However, whether the regulating effect of NK-1R in AR is achieved via RANTES remains unknown.

Methods: In the present study, Sprague-Dawley rats were sensitized and challenged with ovalbumin to make AR models. During the challenge period, the rats were treated intranasally with NK-1R-specific small interfering RNA (siRNA) for NKR group, negative siRNA for NCS group, rats in NSAR group and NS group were given saline. The amount of nasal secretion and the numbers of nose rubs and sneezes were measured in each rat. The levels of NK-1R and RANTES in the nasal mucosal tissues were determined through real-time fluorescence quantitative RT-PCR and immunohistochemical staining. The numbers of eosinophils in the collected nasal lavage fluid (NLF) were counted, and the concentration of RANTES in NLF was determined by enzyme-linked immunosorbent assay.

Results: Compared with that in the NS group, the expression of NK-1R and RANTES was significantly higher in the nasal mucosa of NSAR and NCS group rats. The sneezing and nose rubbing counts and the amount of nasal secretions were increased significantly in the NSAR and NCS groups. Rats in the NKR group experienced greater relief from AR symptoms than rats in the NSAR and NCS groups. Furthermore, knockdown of NK-1R expression also significantly eliminated RANTES expression and eosinophil infiltration in the nasal mucosa of NKR group rats.

Conculsion: For the first time, we show that intranasal treatment with NK-1R-specific siRNA can significantly decrease RANTES expression, AR-related symptoms, and eosinophil inflammation, suggesting that the regulating effect of NK-1R in the development of AR occurs via alteration of RANTES expression.

Background: Extensive data suggest that exposure to cigarette smoke can induce pulmonary epithelial barrier dysfunction. However, the effects of cigarette smoke on the nasal epithelial barrier are still unclear. Here, we investigated the consequence and mechanism of cigarette smoke on the nasal epithelial barrier.

Methods: Sprague Dawley rats were exposed to cigarette smoke for 3 or 6 months, and changes in inflammatory markers and nasal barrier function were evaluated. Moreover, underlying mechanisms were explored. Finally, normal human bronchial epithelial cells were cultured with or without tumor necrosis factor-alpha (TNF-α) in vitro, and the levels of continuity and tight junction-associated proteins were measured.

Results: In vivo experiments showed that the nasal mucosal barrier function of rats exposed to cigarette smoke was disturbed. Indeed, proteins associated with tight junctions were decreased, and the levels of inflammatory factors, such as IL-8, IL-6, and TNF-α, were dramatically increased in comparison to those of control animals. In vitro, TNF-α was shown to disrupt the continuity of proteins associated with tight junctions and to downregulate the expression of these proteins in bronchial epithelial cells.

Conclusions: We found that cigarette smoke disrupted the nasal mucosal barrier, and the extent of the damage was correlated with the duration of cigarette smoke exposure. We showed that TNF-α can disrupt the continuity and attenuate the expression of tight junction proteins in human bronchial epithelial cells. Therefore, cigarette smoke may induce nasal epithelial barrier dysfunction through TNF-α.

Background: Positron emission tomography (PET) scan is a valuable imaging modality widely used in the management of cancers. Its usage is well defined for most head and neck malignancies. However, there is a lack of consensus regarding the utility of PET scan for sinonasal malignancies. This is highlighted by the latest international consensus statement on endoscopic skull base surgery.

Objective: This systematic review aims to clarify the role of PET scan in the management of sinonasal malignancies.

Methods: We conducted a comprehensive literature search using PubMed, MEDLINE, EMBASE, Web of Science, CINAHL, and Cochrane databases for research studies of interest. The Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) updated statement was used to guide the review.

Results: In total, 1807 articles were assessed for eligibility. Thirty-nine original papers, published between 2004 and 2021, met inclusion criteria. Seven articles focused on the role of PET scan for inverted papilloma, 23 for sinonasal carcinoma, 4 for melanoma, and 3 for lymphoma, and finally, 3 articles focused on the use of specific PET scan tracers for sinonasal malignancies. Qualitative summaries for each potential role of PET scans were provided. In general, included studies were retrospective in nature with low level of evidence.

Conclusions: In general, and across all types of sinonasal malignancies, PET scan yielded positive results regarding detection and initial staging. It was also considered as the modality of choice for detection of distant metastases, except in the case of sinonasal lymphoma. PET scan's main limit resides in its inability to detect lesions in or close to the metabolic activity of the brain.

Background: Eosinophilic chronic rhinosinusitis with nasal polyps (Eos-CRSwNP) remains a recalcitrant disease with a high recurrence rate.

Objective: This study aimed to identify a predictor of long-term recurrence in patients with Eos-CRSwNP.

Methods: A total of 39 Eos-CRSwNP patients who had their initial and recurrent nasal polyps surgically removed were retrospectively included in this study, with 49 Eos-CRSwNP patients without recurrence and 32 patients with non-Eos-CRSwNP matched by randomly chosen. Clinical characteristics were compared among or between groups. Spearman correlation analyses and a backward stepwise multivariate logistic regression analysis were performed to find factors associated with the recurrence and recurrence time of Eos-CRSwNP. Furthermore, a receiver operating characteristic (ROC) curve was used to determine the predictor of long-term Eos-CRSwNP recurrence.

Results: The number and ratio of tissue eosinophils were highest in Eos-CRSwNP with recurrence and lowest in non-Eos-CRSwNP. The ratio of tissue lymphocytes was highest in non-Eos-CRSwNP and lowest in Eos-CRSwNP with recurrence, with the number of tissue lymphocytes higher in Eos-CRSwNP without recurrence than the other two groups. The numbers of tissue lymphocytes in the initial nasal polyps were lower and the numbers of tissue eosinophils were higher in the group of recurrent nasal polyps that recurred at >5 years after surgery than in the nasal polyps that recurred at <5 years after surgery. The tissue lymphocyte-to-eosinophil ratio (LER) showed a significant negative correlation with the recurrence and the recurrence time of Eos-CRSwNP. A ROC curve revealed that a tissue LER value < 0.67 predicted long-term Eos-CRSwNP recurrence with 72.73% sensitivity and 82.35% specificity (area under the curve  =  0.789).

Conclusion: Tissue LER is strongly associated with Eos-CRSwNP recurrence and may play a key role in predicting long-term Eos-CRSwNP recurrence.

Objectives: Transplant patients are high risk for surgery due to their immunocompromised state. There is a paucity of evidence concerning the differences in incidence of chronic rhinosinusitis (CRS) in solid versus non-solid organ transplant. Our aim is to analyze the difference in incidence of CRS requiring endoscopic sinus surgery (ESS) between non-solid and solid transplant populations and determine if certain risk factors are associated with increased incidence of recalcitrant CRS in non-solid versus solid transplants.

Study design: Retrospective cohort.

Setting: Multisite tertiary academic center.

Methods: This is a retrospective chart review of 1303 transplant recipients who were seen in our rhinologic clinic for CRS between 2017 and 2022. A total of 224 patients underwent ESS and were further analyzed for risk factors associated with recalcitrant disease requiring sinus surgery. Subgroup analysis based on solid and non-solid organ transplant was performed.

Results: Of the 224 patients in the study, 171/224 (76.3%) had solid transplants while 53/224 (23.6%) had non-solid transplants. 17.19% of all transplant recipients required ESS. The incidence of ESS in non-solid transplants was 28.2% versus 57% in solid transplant. The risk of recalcitrant CRS in solid transplant recipients was almost 1.78 times greater than those with non-solid organ transplant (95% CI, 1.27-2.54, p  =  0.0005). Individual factors such as certain immunotherapy drugs, pancytopenia, and rejection appear to correlate with the risk of ESS in both non-solid and solid organ transplant.

Conclusion: Risk of ESS was greater in the solid transplant recipients compared to those who received non-solid organ transplant.

Background: Middle meatal antrostomy (MMA) is the traditional intervention for chronic maxillary sinusitis but often fails to correct a nonfunctioning maxillary sinus that has lost its capability for mucociliary clearance. Endoscopic-modified medial maxillectomy (EMMM) can reshape the maxillary sinus and avoid a "sumping" effect, preventing secondary bacterial colonization, encouraging dependent drainage, and promoting effective nasal irrigation.

Objectives: We describe a modification of the EMMM surgical technique in patients with recalcitrant maxillary sinusitis and perioperative outcomes.

Methods: Consecutive adult patients with nonfunctioning maxillary sinuses managed with EMMM were assessed. Primary outcomes were the resolution of the presenting symptom and the absence of mucostasis. Secondary outcomes were early (<90 days) and late (>90 days) morbidity.

Results: Fifty-seven patients (51.7  ±  17.5 years, 56.1% female) were assessed. Fifty-two patients had complete resolution of their presenting symptom (91.2% [95% CI: 80.7-97.1]) and 52 patients had an absence of mucostasis (91.2% [95% CI: 80.7-97.1]). Those with persistent crusting were also those with symptoms. Early morbidities included temporary dysesthesia (3.2%), bleeding (1.1%), and pain (3.2%), with no late morbidities.

Conclusion: EMMM is a robust approach for salvaging a nonfunctioning maxillary sinus. The procedure enhances nasal irrigation, supplants mucociliary clearance, and discourages dependent mucus retention.