Summary PhenoAge acceleration consistently associates with incident CRSwNP and CRSsNP, but not AR. Accelerated biological aging mediates 19.5% and 26.4% of smoking's pathogenic effects on CRSsNP and CRSwNP, respectively.

Tertiary lymphoid structures (TLSs) are ectopic lymphoid aggregates that form in or in close proximity to tumors and other chronically inflamed tissues, where they serve as crucial sites for local antigen presentation, lymphocyte priming, and adaptive immune coordination. Increasing evidence across diverse cancers supports TLSs as key modulators of antitumor immunity, correlating with improved patient prognosis and response to immune checkpoint blockade. Yet, TLSs exhibit striking spatiotemporal and functional heterogeneity—ranging from immune-stimulatory to immune-suppressive—which complicates their clinical interpretation and therapeutic targeting. Recent studies have focused on elucidating the molecular cues driving TLS induction, the mechanisms regulating their maturation, and their dynamic interactions with the tumor microenvironment. In this review, we provide an integrated overview of these advances and discuss the clinical and translational implications of TLSs as prognostic biomarkers and immunotherapeutic targets.

Lung cancer remains the leading cause of cancer-related mortality worldwide, with limited treatment efficacy and frequent resistance to conventional therapies. Recent advances have uncovered the critical influence of the human microbiota—complex communities of bacteria, viruses, fungi, and other microorganisms—on lung cancer pathogenesis and therapeutic responses. This review synthesizes current knowledge on the compositional and functional roles of microbiota across multiple body sites, including the gut, lung, tumor microenvironment, circulation, and oral cavity, highlighting their contributions to tumor initiation, progression, metastasis, and immune regulation. We emphasize the bidirectional communication between microbial metabolites and host immune pathways, particularly the gut–lung axis, which modulates systemic and local antitumor immunity. Importantly, microbiota composition has been linked to differential responses and toxicities in chemotherapy, radiotherapy, targeted therapy, and immune checkpoint blockade. Microbiota-targeted interventions, such as probiotics, fecal microbiota transplantation, and selective antibiotics, show promising potential to enhance treatment efficacy and mitigate adverse effects. However, challenges remain in clinical translation due to interindividual microbiome variability, mechanistic complexities, and limited longitudinal data. Future research integrating multi-omics, microbial functional profiling, and controlled clinical trials is essential to harness the microbiome as a precision medicine tool in lung cancer management. This review provides a comprehensive overview of the emerging role of microbiota in lung cancer development and therapy, offering new perspectives for innovative therapeutic strategies.

IntroductionViral infections have been implicated as a risk factor for laryngeal cancer. Given the possible effects of Corona virus disease 2019 (COVID-19) on the laryngeal tissue, we investigated the causal link between COVID-19 and laryngeal cancer using a two-sample Mendelian randomization (MR) approach.MethodsWe utilized genetic data from the 5th Genome-wide association studies (GWAS) edition of the COVID-19 Host Genetics Initiative (published on January 18, 2021) and a large-scale laryngeal cancer GWAS comprising 180 cases and 218,612 controls of European ancestry. We applied inverse variance weighting, MR Egger, and weighted median methods to infer causality. We performed sensitivity analysis using the “leave-one-out” method to verify robustness.ResultsWe found no evidence of a causal association between gene-predicted COVID-19 and laryngeal cancer [Odds ratio (OR)=0.24 (95% Confidence intervals (CI), 0.05–1.26), P=0.09]. However, we observed significant inverse associations between gene-predicted COVID-19 hospitalization [OR=0.51 (95% CI, 0.28–0.95), P=0.03] and severe patients [OR=0.62 (95% CI, 0.43–0.90), P=0.01] and laryngeal cancer. Notably, the study detected important genetic variants, such as rs13050728, that modulate the expression of interferon alpha receptor 2 (IFNAR2), indicating possible roles for immune response pathways in both COVID-19 and cancer.DiscussionThis study reveals a potential interaction between COVID-19 severity, genetic factors, and laryngeal cancer, underscoring the importance of investigating the immune response mechanisms in both conditions. These findings contribute to the understanding of the complex interactions between COVID-19 and laryngeal cancer and may guide future research on the role of immune response, particularly involving IFNAR2.

Langerhans cell histiocytosis (LCH) is a neoplastic disease characterized by aberrant proliferation of the mononuclear phagocyte system, predominantly affecting children under the age of 3 years. Although LCH can affect almost all organs, sinus involvement is rare. This case report documents a 9-year-old boy presented with vision impairment and intermittent headache on the right side. The CT scan and MRI examination revealed the presence of a soft mass in the right atrium of sphenoid sinus, which impacted the right optic canal. Biopsy results confirmed the presence of LCH. Considering the involvement of optic canal and vision impairment, meticulous debridement was performed followed by a 12-month standard chemotherapy. After 2 years of follow-up, the patient showed significant improvement, despite the presence of an encapsulated cyst in the right sphenoid sinus. This case highlights the importance of considering LCH when encountering an isolated soft mass accompanied by decreased vision in the sphenoid sinus. A thorough physical examination, laboratory tests, and imaging methods should be performed, with a biopsy being necessary to confirm the type of lesion and guide the appropriate treatment.

BACKGROUND:Identifying predictive biomarkers for allergen immunotherapy response is crucial for enhancing clinical efficacy. This study aims to identify such biomarkers in patients with allergic rhinitis (AR) undergoing subcutaneous immunotherapy (SCIT) for house dust mite allergy. METHODS:The Tongji (discovery) cohort comprised 72 AR patients who completed 1-year SCIT follow-up. Circulating T and B cell subsets were characterized using multiplexed flow cytometry before SCIT. Serum immunoglobulin levels and combined symptom and medication score (CSMS) were assessed before and after 12-month SCIT. Responders, exhibiting ≥30% CSMS improvement, were identified. The random forest algorithm and logistic regression analysis were used to select biomarkers and establish predictive models for SCIT efficacy in the Tongji cohort, which was validated in another Wisco cohort with 43 AR patients. RESULTS:Positive SCIT response correlated with higher baseline CSMS, allergen-specific IgE (sIgE)/total IgE (tIgE) ratio, and frequencies of Type 2 helper T cells, Type 2 follicular helper T (TFH2) cells, and CD23+ nonswitched memory B (BNSM) and switched memory B (BSM) cells, as well as lower follicular regulatory T (TFR) cell frequency and TFR/TFH2 cell ratio. The random forest algorithm identified sIgE/tIgE ratio, TFR/TFH2 cell ratio, and BNSM frequency as the key biomarkers discriminating responders from nonresponders in the Tongji cohort. Logistic regression analysis confirmed the predictive value of a combination model, including sIgE/tIgE ratio, TFR/TFH2 cell ratio, and CD23+ BSM frequency (AUC = 0.899 in Tongji; validated AUC = 0.893 in Wisco). CONCLUSIONS:A T- and B-cell signature combination efficiently identified SCIT responders before treatment, enabling personalized approaches for AR patients.

Proton-activated G protein-coupled receptors (GPCRs), initially discovered by Ludwig in 2003, are widely distributed in various tissues. These receptors have been found to modulate the immune system in several inflammatory diseases, including inflammatory bowel disease, atopic dermatitis, and asthma. Proton-activated GPCRs belong to the G protein-coupled receptor family and can detect alternations in extracellular pH. This detection triggers downstream signaling pathways within the cells, ultimately influencing the function of immune cells. In this review, we specifically focused on investigating the immune response of proton-activated GPCRs under inflammatory conditions.

BACKGROUND:Angiogenesis has great potential in the treatment of acute limb ischemia (ALI). Here, we aimed to investigate the effect and mechanism of Aryl hydrocarbon receptor (AhR) on angiogenesis in ALI.METHODS:The ALI mouse model was constructed by femoral artery ligation, and the cell ischemia injury was induced by Hypoxia/serum deprivation. The laser doppler perfusion imaging was executed to detect the limb blood flow velocity. The tube formation assay was performed to evaluate angiogenesis. The cell viability was measured by 3-(45)-dimethylthiahiazo(-z-y1)-35-di-phenytetrazoliumromide. The cell migration was detected by wound healing assay. Hematoxylin-eosin, immunohistochemistry, immunofluorescence, dual-luciferase reporter gene assay, and Chromatin immunoprecipitation assay were conducted.RESULTS:In ALI models, AhR expression was increased and translocated from cytoplasm to nucleus. Besides, necrosis and inflammatory infiltration were also increased in gastrocnemius tissues of model mice. In addition, AhR loss (LV-sh-AhR) promoted cell viability, angiogenesis, and migration, and also elevated the levels of vascular endothelial growth factor (VEGF), Tie2, and Ang2 in HUVEC models with Hypoxia/serum deprivation injury. Meanwhile, the interaction between AhR and signal transducer and activator of transcription 1 (STAT1), as well as STAT1 and VEGF, has also been confirmed. Co-transfection of LV-sh-AhR and LV-STAT1 suppressed cell viability, angiogenesis, and migration of injured HUVECs. Furthermore, injection of AAV2/9-shAhR in vivo also promoted angiogenesis, which was consistent with the in vitro experimental results.CONCLUSIONS:In ALI models, activated AhR was translocated to the nucleus and down-regulated VEGF expression by promoting the transcriptional activity of STAT1, thereby inhibiting endothelial angiogenesis.

Although the expression of Mex3 RNA-binding family member B (MEX3B) is upregulated in human nasal epithelial cells (HNECs) predominately in the eosinophilic chronic rhinosinusitis (CRS) with nasal polyps (CRSwNP) subtype, its functions as an RNA binding protein in airway epithelial cells remain unknown. Here, we revealed the role of MEX3B based on different subtypes of CRS and demonstrated that MEX3B decreased the TGF-β receptor III (TGFBR3) mRNA level by binding to its 3′ UTR and reducing its stability in HNECs. TGF-βR3 was found to be a TGF-β2–specific coreceptor in HNECs. Knocking down or overexpressing MEX3B promoted or inhibited TGF-β2–induced phosphorylation of SMAD2 in HNECs, respectively. TGF-βR3 and phosphorylated SMAD2 levels were downregulated in CRSwNP compared with controls and CRS without nasal polyps with a more prominent downregulation in the eosinophilic CRSwNP. TGF-β2 promoted collagen production in HNECs. Collagen abundance decreased and edema scores increased in CRSwNP compared with control, again more prominently in the eosinophilic type. Collagen expression in eosinophilic CRSwNP was negatively correlated with MEX3B but positively correlated with TGF-βR3. These results suggest that MEX3B inhibits tissue fibrosis in eosinophilic CRSwNP by downregulating epithelial cell TGFBR3 expression; consequently, MEX3B might be a valuable therapeutic target against eosinophilic CRSwNP.

Background: Glucose concentrations are increased in nasal secretions in chronic rhinosinusitis (CRS). However, the glucose metabolism and its contribution to disease pathogenesis in CRS remain unexplored. Objectives: We sought to explore the glucose metabolism and its effect on the function of nasal epithelial cells in CRS with and without nasal polyps (CRSwNP and CRSsNP). Methods: Glucose metabolites were detected with mass spectrometry. The mRNA levels of glucose transporters (GLUTs), metabolic enzymes, and inflammatory mediators were detected by quantitative RT-PCR. The protein expression of GLUTs was studied by immunofluorescence staining, Western blotting, and flow cytometry. Glucose uptake was measured by using fluorescent glucose analog. Human nasal epithelial cells (HNECs) were cultured. Bioenergetic analysis was performed with Seahorse XF analyzer. Gene expression in HNECs was profiled by RNA sequencing. Results: Increased glucose concentrations in nasal secretions was confirmed in both CRSsNP and CRSwNP. GLUT4, GLUT10, and GLUT11 were abundantly expressed in HNECs, whose expression was upregulated by inflammatory cytokines and D-glucose and was increased in CRS. Glucose uptake, glycolysis and tricarboxylic acid cycle metabolites, metabolic enzymes, and extracellular acidification rate and oxygen consumption rates were increased in HNECs in CRSsNP and CRSwNP, with a predominant shift to glycolysis. HNECs treated with high-level apical D-glucose showed enhanced glucose uptake, predominant glycolysis, and upregulated production of IL-1a, IL-1b, TNF-a, CCL20, and CXCL8, which was suppressed by 2-deoxy-D-glucose, an inhibitor of glycolysis. Conclusions: Increased glucose in nasal secretions promotes glucose uptake and predominant glycolysis in epithelial cells, augmenting the proinflammatory function of epithelial cells in CRS. (J Allergy Clin Immunol 2023;151:991-1004.)

Objective To identify factors affecting the efficacy of steroid-eluting sinus stents implanted after endoscopic sinus surgery (ESS) in patients with chronic rhinosinusitis with nasal polyps (CRSwNP). Methods We performed a post-hoc analysis of a randomized self-controlled clinical trial on post-operative implantation of bioabsorbable steroid-eluting stents in patients with CRSwNP. Univariate logistic regression analysis was conducted to identify which of the following factors affect the response to post-operative stent implantation: sex, serum eosinophil levels, history of prior surgery, endoscopic scores, and comorbid conditions (asthma and allergic rhinitis). The primary outcome was the rate of post-operative intervention on day 30, and the secondary outcome was the rate of polypoid tissue formation (grades 2–3) on days 14, 30, and 90. Results A total of 151 patients with CRSwNP were included in the post-hoc analysis. Asthma was identified as the only risk factor for a poor response to steroid-eluting sinus stents on post-operative day 30, with an odds ratio of 23.71 (95% CI, 2.81, 200.16; P =0.004) for the need for post-operative intervention and 19 (95% CI, 2.20, 164.16; P =0.003) for moderate-to-severe polypoid tissue formation. In addition, the asthmatic group showed higher rates of post-operative intervention and polypoid tissue formation than the non-asthmatic group on post-operative day 30. Blood eosinophil levels were not identified as a risk factor for poor outcomes after stent implantation. Conclusion Comorbid asthma, but not blood eosinophil level, impairs the efficacy of steroid-eluting sinus stents in the short term after ESS in patients with CRSwNP.

Background Pharynx and larynx cancers (PLCs) are the top killer cancers in head and neck and significantly affect the quality of life of patients. A detailed study examining the disease burden and risk factors of PLCs is lacking. Methods Data on mortality and disability-adjusted life-years (DALYs) were extracted from the Global Burden of Disease Study 2019. The estimated annual percentage change (EAPC) of the age-standardized mortality rate was calculated using a generalized linear model with a Gaussian distribution. Mortality and DALYs were stratified according to the sociodemographic index (SDI), age, gender, and risk factors. The association between the SDI and mortality rate was measured using Spearman’s correlation. Results Between 1990 and 2019, the total number of deaths due to PLCs increased by 60.7% (95% confidence intervals: 39.32 to 66.8), from 192.38 thousand in 1990 to 309.16 thousand in 2019, and the total DALYs due to PLCs increased by 49.41% (95% confidence intervals: 30.15 to 53.27), from 5.91 million in 1990 to 8.83 million in 2019. The age-standardized mortality rate declined for larynx cancer (from 2.19 in 1990 to 1.49 in 2019) and nasopharynx cancer (1.26 to 0.86) but increased slightly for other pharynx cancer (1.25 to 1.37). The death number of PLCs was significantly higher in men aged 50 to 70 years, which accounts for 46.05% and 43.83% of the total deaths in 1990 and 2019, respectively. Low and low-middle countries had the greatest age-standardized mortality rate for larynx and other pharynx cancer, while low-middle and middle countries dominated for nasopharynx cancer. The leading risk factors for PLCs were smoking and alcohol use, which account for 37.92% and 58.84% in total DALYs rate of PLCs, and the influence of risk factors was significant in men. Conclusion The total number of deaths and DALYs due to PLCs increased from 1990 to 2019. Countries with relatively low SDI and middle-aged and older men had the greatest burden of PLCs. Building better health care systems in relatively low SDI countries and improving strategies of smoking and alcohol control should be a priority in health policy.

Background Although subsequent anti-inflammatory treatments are indispensable for patients with chronic rhinosinusitis (CRS) undergoing sinus surgery, few studies have explored the factors influencing the efficacy of postoperative anti-inflammatory treatment. Objective We aimed to develop prediction models for the response to glucocorticoid- and macrolide-based postoperative therapy in CRS patients. Methods We performed a post-hoc analysis of our previous study comparing the efficacy of fluticasone propionate and clarithromycin in the postoperative treatment of CRS patients. Clinical characteristics and treatment outcome information were collected. In addition, diseased sinonasal mucosal tissues obtained during surgery were processed for Bio-Plex analysis of protein levels of 34 biomarkers. Classification trees were built to predict refractory CRS based on clinical characteristics and biological markers for patients treated with fluticasone propionate or clarithromycin. A random forest algorithm was used to confirm the discriminating factors that formed the classification trees. Results One year after surgery, 22.7% of the patients (17/75) treated with fluticasone propionate, and 24.3% of those (18/74) treated with clarithromycin were diagnosed with refractory CRS. Nasal tissue IL-8 and IgG3 levels and headache VAS scores in the fluticasone propionate group, and nasal tissue IgG4 levels and overall burden of symptoms VAS scores in the clarithromycin group, were identified as discriminating factors forming the classification tree to predict refractory CRS. The overall predictive accuracy of the model was 89.3% and 87.8% for fluticasone propionate- and clarithromycin-based postsurgical treatment, respectively. Conclusions Classification trees built using clinical and biological parameters could be helpful in identifying patients with poor response to fluticasone propionate- and clarithromycin-based postoperative treatment.

目的:探讨中频刺激眼部瞳子髎穴位对轻中度近视合并眼压增高患者的治疗效果及可能机制.方法:取2019年1-5月在我院就诊并符合《近视眼学》轻中度近视合并眼压增高的相关诊断标准的近视患者260例,随机分为两组,对照组120例与观察组140例.对照组给予患者矫治镜,纠正不良用眼习惯,注意眼卫生,做眼保健操与眼肌训练,观察组在对照组基础上用中频眼部治疗仪对准瞳子髎进行中频治疗,每次20 min,2次/d,5 d/周,20 d为一个疗程,共3个疗程.检测所有患者治疗前后的屈光度、视力、非接触眼压(Intraocular Pressure,IOP)、生物力学校正眼压(Biomechanically Intraocular Pressure,bIOP)、调节灵活度与调节幅度,记录两组患者的疗效与不良反应.结果:治疗前,两组患者的屈光度、视力、IOP、bIOP、调节灵活度与调节幅度差异无统计学意义(P>0.05),治疗后,两组患者的屈光度、视力、调节灵活度与调节幅度均明显增高(P<0.05),IOP与bIOP均有不同程度地降低;与对照组比,观察组的屈光度、视力、调节灵活度与调节幅度增高明显(P<0.05),IOP与bIOP明显降低(P<0.05).与对照组比,观察组的总有效率较高(P<0.05),两组患者的治疗期间未发生明显的不良反应.结论:中频刺激瞳子髎穴位可用于治疗轻中度近视合并眼压增高患者,在改善屈光度、IOP、bIOP、调节灵活度与调节幅度方面具有一定优势.

AbstractBackgroundThe role of endoplasmic reticulum (ER) stress in the pathogenesis of allergic rhinitis (AR) remains elusive.MethodsReal‐time polymerase chain reaction (RT‐PCR), immunohistochemistry, and western blotting analyses were performed to detect the expression of ER stress and unfolded protein response markers: 78‐kDa glucose‐regulated protein (GRP78), C/EBP homologous protein (CHOP), activating transcription factor 6 (ATF6α), spliced X‐box binding protein 1 (sXBP‐1), and phosphorylated eukaryotic initiation factor 2α (p‐eIF2α), in inferior turbinate tissue samples from patients with AR and non‐AR controls. Nasal tissues from patients with AR were cultured ex vivo and treated with 4‐phenylbutyric acid (4‐PBA), an ER stress inhibitor.ResultsCompared to those in non‐AR controls, the mRNA and protein levels of GRP78, CHOP, ATF6α, sXBP‐1, and p‐eIF2α were significantly increased in nasal tissues from patients with AR. GRP78 and CHOP were mainly expressed in CD138+ plasma cells in nasal tissues from patients with AR. The frequency of IgE+CD138+ plasma cells was significantly higher in nasal tissues from patients with AR than that in non‐AR controls. IgE levels in nasal secretions and tissues were positively correlated with GRP78 and CHOP mRNA levels in the nasal tissues. After 4‐PBA treatment, the protein expression of GRP78, CHOP, ATF6α, sXBP‐1, and p‐eIF2α was significantly reduced in cultured AR‐derived nasal tissues, and IgE levels were simultaneously decreased in cultured supernatants.ConclusionsER stress may be involved in the regulation of local IgE production in patients with AR. Inhibition of ER stress potentially provides a therapeutic avenue in AR by reducing local IgE production.Level of EvidenceNA

目的 探究ICL植入术与全飞秒激光术矫正高度近视术AC/A的效果.方法 选取2017年10月至2018年10月于本院行手术矫正的高度近视患者42例(78眼),根据矫正手术的不同分为两组,将行全飞秒激光术的20例纳入对照组(39眼),将行ICL植入术的22例纳入研究组(39眼),通过术后随访,比较两组视觉质量、AC/A值.结果 研究组视觉质量指标UCVA、BCVA、有效性指数、安全性指数均优于对照组(P<0.05);术后研究组AC/A值低于对照组(P<0.05).结论 针对高度近视患者ICL植入术和全飞秒激光术均可纠正视觉质量,与全飞秒激光术相比,ICL植入术治疗效果更佳,视觉质量、AC/A、有效性系数等均更优.

Background Although immune checkpoint inhibitor (ICI) therapy has revolutionized the treatment of nasopharyngeal carcinoma (NPC), it is still the second- or third-line treatment after the failure of radiotherapy or chemotherapy. In this study, we aimed to investigate the impact of concurrent chemoradiotherapy (CCRT) on programmed death-ligand 1 (PD-L1) protein expression in NPC patients. Methods We enrolled 24 NPC patients treated with intensity-modulated radiation therapy (IMRT) combined with cisplatin CCRT. PD-L1 expression was evaluated by immunohistochemistry, and next-generation sequencing and annotation were performed to determine the genetic alteration after CCRT. Results Our results showed that patients with a high expression of PD-L1 were more inclined to a complete response (CR) to chemoradiotherapy, as opposed to a partial response (PR) (P<0.05). Moreover, the mean values of the tumor mutation burden (TMB) and the tumor neoantigen burden (TNB) in the PD-L1 positive group were significantly lower than that of the PD-L1 negative group in our cohort. Conclusions We confirmed that the TMB and TNB may be potential clinical indicators in NPC treatment, and PD-L1 expression may be a clinical biomarker in NPC chemoradiotherapy. Finally, through next-generation sequencing and annotation, we found that the most frequent driver gene mutations in NPC were TET2, TP53, and MAPK.

BACKGROUND:Cold-inducible RNA-binding protein (CIRP) is a newly identified damage-associated molecular pattern molecule. Its roles beyond promoting inflammation and in human diseases are poorly understood. This study aimed to investigate the involvement of CIRP in chronic rhinosinusitis with nasal polyps (CRSwNP).METHODS:Immunohistochemistry, quantitative RT-PCR, and ELISA were used to detect the expression of CIRP and matrix metalloproteinases (MMPs) in sinonasal mucosal samples and nasal secretions. Human nasal epithelial cells (HNECs) and THP-1 cells, a human monocytic/macrophage cell line, were cultured to explore the regulation of CIRP expression and MMP expression.RESULTS:Cytoplasmic CIRP expression in nasal epithelial cells and CD68+ macrophages in sinonasal tissues, and CIRP levels in nasal secretions were significantly increased in both patients with eosinophilic and noneosinophilic CRSwNP as compared to those in control subjects. IL-4, IL-13, IL-10, IL-17A, TNF-α, Dermatophagoides pteronyssinus group 1, and lipopolysaccharide induced the production and secretion of CIRP from HNECs and macrophages differentiated from THP-1 cells. CIRP promoted MMP2, MMP7, MMP9, MMP12, and vascular endothelial growth factor A (VEGF-A) production from HNECs, macrophages differentiated from THP-1 cells, and polyp tissues, which was inhibited by the blocking antibody for Toll-like receptor 4, but not advanced glycation end products. The expression of MMPs and VEGF-A in tissues correlated with CIRP levels in nasal secretions in patients with CRSwNP.CONCLUSIONS:The upregulated production and release of CIRP from nasal epithelial cells and macrophages may contribute to the edema formation in both eosinophilic and noneosinophilic CRSwNP by inducing MMP and VEGF-A production from epithelial cells and macrophages.

Purpose Plasma cells and immunoglobulins (Igs) play a pivotal role in the induction and maintenance of chronic inflammation in nasal polyps. During secondary immune responses, plasma cell survival and Ig production are regulated by the local environment. The purpose of the present study was to investigate the presence of long-lived plasma cells (LLPCs) and specific survival niches for LLPCs in human nasal polyps. Methods Nasal mucosal samples were cultured with an air-liquid interface system and the Ig levels in culture supernatants were analyzed by enzyme-linked immunosorbent assay. The characteristics of LLPCs in nasal polyps were determined by immunohistochemistry and immunofluorescence. The expression of neurotrophins as well as their receptors was detected by quantitative real-time polymerase chain reaction, immunohistochemistry, immunofluorescence, and Western blotting. Results The numbers of CD138+ total plasma cells and BCL2+ plasma cells were increased in both eosinophilic and non-eosinophilic nasal polyps compared with those in normal tissues. The production of IgG, IgA, and IgE was detected in culture supernatants even after a 32-day culture of nasal polyps. Although the total numbers of plasma cells were decreased in nasal polyps after culture, the numbers of BCL2+ plasma cells remained stable. The expression of nerve growth factor (NGF) as well as tropomyosin receptor kinase (Trk) A, a high-affinity receptor for NGF, was upregulated in both eosinophilic and non-eosinophilic nasal polyps. In addition, BCL2+ plasma cell numbers were positively correlated with NGF and TrkA mRNA expression in nasal mucosal tissues. Polyp plasma cells had the expression of TrkA. Conclusions Human nasal polyps harbor a population of LLPCs and NGF may be involved in their prolonged survival. LLPCs may be a novel therapeutic target for suppressing the local Ig production in nasal polyps.