鼻息肉中HIF-1α、VEGF 和miR-200a 表达及其与复发相关性研究

目的:分析不同病理分型鼻息肉中HIF-1α、VEGF和miR-200a表达及其与复发相关性研究。方法:选取鼻息肉患者42例,在随访期间有15例鼻息肉复发。采用免疫组化SABC法检测鼻息肉及下鼻甲组织中HIF-1α、VEGF表达水平,采用q RT-PCR技术检测鼻息肉及下鼻甲粘膜组织中miRNA-200a表达量。对比分析不同病理分型HIF-1α、VEGF、miRNA-200a表达差异并分析鼻息肉复发的因素。结果:鼻息肉中miR-200a表达量明显低于下鼻甲粘膜组织(P0.05)。鼻息肉中HIF-1α、VEGF表达量明显高于于下鼻甲粘膜组织(P0.05)。鼻息肉病组织中miR-200a表达量明显低于单发鼻息肉、多发鼻息肉(P0.05);鼻息肉病标本中HIF-1α、VEGF表达量明显高于单发鼻息肉、多发鼻息肉组织(P0.05)。鼻息肉复发与鼻息肉的病理分型、HIF-1α、VEGF表达密切相关(P0.05)。结论:鼻息肉增生和局部血管的生成密切相关,HIF-1α可能是同构调节miR-200a表达,来控制VEGF及血管生成的。     

体外红霉素对鼻息肉组织中eotaxin的作用

目的:观察红体外霉素对体外培养鼻息肉组织中嗜酸性粒细胞趋化因子(eotaxin)的作用。方法:从27例住院病人鼻腔中各取鼻息肉标本一份,将每一份均分4份,分对照组、红霉素组培养1d、3d后。每组各取鼻息肉标本经逆转录聚合酶链式反应(RT-PCR)与免疫组织化学染色检测eotaxin表达。结果:①红霉素组中鼻息肉的eotaxinmRNA光度值较对照组低(p<0.05);②两组鼻息肉中eotaxin蛋白灰度值比较,在培养1d后无明显差异,但培养3d后,红霉素组eotaxin蛋白灰度值较对照组低(p<0.05)。结论:体外红霉素能抑制鼻息肉中eotaxin表达,对鼻息肉的临床治疗有指导作用。     

鼻息肉中NF-κB的活化对IL-8转录的影响及意义

目的 通过检测鼻息肉组织中核因子кB(NF-кB)的活化及白介素-8(IL-8)的转录水平,探讨鼻息肉组织中NF-кB的活化对IL-8转录的影响及临床意义.方法分别应用凝胶电泳迁移实验法、蛋白免疫印迹法、免疫组织化学法及逆转录聚合酶链反应法检测47例鼻息肉患者(鼻息肉组)的息肉组织中NF-κB的活性及其p65亚基蛋白水平、IL-8的组织定位及转录水平;以22例鼻中隔手术患者中鼻甲黏膜组织作为阴性对照(对照组);对NF-кB的活性及其p65亚基蛋白水平与IL-8的转录水平进行Pearson's相关性分析.结果 EMSA测得鼻息肉组患者息肉组织中NF-κB的活性(216.51±17.33)较对照组(63.57±5.26)显著增高(P<0.01);Western Blot 测得鼻息肉组NF-κB亚基p65 蛋白的水平(153.72±9.15)较对照组(73.92±6.74)显著增高(P<0.05);半定量RT-PCR 测得IL-8 mRNA的转录水平(0.95±0.08)也显著高于对照组(0.23±0.03)(P<0.05);Pearson's相关性分析结果提示:鼻息肉组患者息肉组织中NF-κB的活性及其p65亚基蛋白水平与IL-8的转录水平呈显著正相关性(r值分别为 0.78 & 0.53,均P<0.01).结论 IL-8是鼻息肉组织中NF-кB激活后所分泌的重要的炎性细胞因子,NF-кB和IL-8引起的局部微环境的改变可能是鼻息肉发病的重要因素.     

鼻内窥镜鼻窦手术168例临床分析

慢性鼻窦炎,鼻息肉是鼻科常见病之一,虽然不会直接威胁患者的生命,但却影响他们的生活质量。近年来不断完善的鼻内窥镜技术,具有视野清晰、明亮、手术微创等优点,为慢性鼻窦炎、鼻息肉的治疗提供了一个简便而有效的手段。现对2001～2003年行鼻内窥镜手术的168例慢性鼻窦炎、鼻息肉患者进行临床分析。     

慢性鼻窦炎鼻息肉行鼻内镜手术并发症的预防与护理分析

目的:研究并分析慢性鼻窦炎鼻息肉行鼻内镜手术并发症的预防与护理措施。方法:将2013年8月~2015年2月在我院入院治疗的112例鼻窦炎与鼻息肉患者纳入到本研究,采用系统性的并发症预防与护理措施,对患者进行6个月的随访,统计术后恢复情况。结果:随访结果显示,112例患者中,81例症状完全消除,29例患者好转,2例患者在术后出现结膜水肿与眼睑青紫的问题,经过针对性的处理后,均恢复正常,疗效满意。结论:对于慢性鼻窦炎鼻息肉实施鼻内镜手术的患者,采用综合性的预防护理干预措施可以显著降低患者并发症发生率,提高护理依从性,值得在临床中推广和使用。     

嗜酸性粒细胞、调节性T细胞对慢性鼻窦炎伴鼻息肉的诊断及预后预测价值分析

摘要 目的：探讨嗜酸性粒细胞、调节性T细胞对慢性鼻窦炎伴鼻息肉的诊断及预后预测价值。方法：选取我院2020年3月到2023年3月收治的100例慢性鼻窦炎伴鼻息肉患者作为研究对象,将其分为慢性鼻窦炎伴鼻息肉组,选取同期来我院治疗的100例单纯慢性鼻窦炎患者作为慢性鼻窦炎组,另选取同期来我院体检的100名健康志愿者作为对照组。对比三组受检者嗜酸性粒细胞、调节性T细胞表达水平,并建立受试者工作特征（ROC）曲线,分析嗜酸性粒细胞、调节性T细胞对慢性鼻窦炎伴鼻息肉的诊断效能。随后对100例性鼻窦炎伴鼻息肉患者手术治疗后进行1年随访,依照患者的复发情况评价其预后情况,并分为两个亚组,将术后1年内复发的21例患者分为预后不良组,两未复发的79例患者分为预后良好组,对比两组患者一般临床情况,嗜酸性粒细胞、调节性T细胞表达水平,并分析嗜酸性粒细胞、调节性T细胞对慢性鼻窦炎伴鼻息肉的预后预测价值。结果：三组受检者嗜酸性粒细胞、调节性T细胞表达水平对比差异显著,慢性鼻窦炎伴鼻息肉组患者嗜酸性粒细胞（EOS）个数高于慢性鼻窦炎组和对照组,调节性T细胞（Tregs）水平低于慢性鼻窦炎组和对照组（P＜0.05）;通过绘制ROC曲线,确定EOS、Tregs其对慢性鼻窦炎伴鼻息肉的诊断效能,结果显示,EOS、Tregs两者联合对慢性鼻窦炎伴鼻息肉的诊断效能优于单一检测（P＜0.05）;预后良好组与预后不良组患者性别、年龄、BMI、吸烟史、饮酒史、白细胞介素-35（IL-35）、转化生长因子-β（TGF-β）、白细胞介素-1β（IL-1β）表达水平对比无明显差异（P＞0.05）,预后良好组与预后不良组患者病程、合并哮喘、合并变应性鼻炎、组织淋巴细胞占比、白细胞介素-10（IL-10）、肿瘤坏死因子-α（TNF-α）、EOS个数以及Tregs表达水平对比差异显著（P＜0.05）;logistic回归分析结果表明：合并哮喘、组织淋巴细胞占比、EOS个数以及Tregs为慢性鼻窦炎伴鼻息肉的预后独立影响因素（P＜0.05）。结论：嗜酸性粒细胞、调节性T细胞不仅对慢性鼻窦炎伴鼻息肉的临床诊断具有重要价值,而且能够预测慢性鼻窦炎伴鼻息肉患者的预后情况,因此临床上对于EOS个数增加,Tregs降低的患者要及时改善治疗措施,预防患者预后不良的发生。     

慢性鼻病中乏氧诱导因子与5-脂加氧酶表达变化及其与疾病严重程度关系研究

摘要 目的：探究慢性鼻病中乏氧诱导因子（HIF-1α）与5-脂加氧酶（5-LOX）表达变化及其与疾病严重程度关系。方法：选取我院2019年7月-2020年11月期间收治的75例慢性鼻病患者作为研究对象;其中鼻息肉25例,变态反应性鼻炎25例,鼻窦炎25例;同期选择30例经鼻中隔偏曲矫正下鼻甲成形术患者的下鼻甲黏膜组织设为对照组。比较四组患者乏氧诱导因子与5-脂加氧酶蛋白及mRNA水平;并分析在不同鼻部疾病中,HIF-1α、5-LOX的相关性。结果：鼻息肉组、变态反应性鼻炎组、鼻窦炎组患者HIF-1α、5-LOX表达水平高于对照组（P<0.05）;鼻息肉组、变态反应性鼻炎组、鼻窦炎组患者HIF-1α、5-LOX表达水平比较无统计学意义（P>0.05）。鼻息肉组、变态反应性鼻炎组、鼻窦炎组患者HIF-1α、5-LOX mRNA表达水平高于对照组（P<0.05）;鼻息肉组、变态反应性鼻炎组、鼻窦炎组患者HIF-1α、5-LOX mRNA表达水平比较无统计学意义（P>0.05）。Parman相关分析,在不同鼻部疾病中,HIF-1α蛋白表达与5-LOX蛋白表达呈正相关（P<0.05）。结论：在慢性鼻病（鼻息肉、变态反应性鼻炎、鼻窦炎）中,HIF-1α、5-LOX表达水平显著升高,且在慢性疾病发展中可能相互促进、互相影响。     

人细胞间粘附分子1基因功能区Ⅰ、Ⅱ的克隆及高效表达

近几年的研究已表明,鼻息肉是一种以嗜酸性细胞浸润为主的鼻粘膜慢性炎症,如果抑制了嗜酸性细胞浸润,也就抑制了鼻息肉的生长。因而对嗜酸性细胞的生物学作用研究受到重视。在嗜酸性细胞选择性粘附、游走和聚集局     

功能性鼻内窥镜手术治疗鼻窦炎与鼻息肉的疗效分析

目的:探讨功能性鼻内窥镜手术治疗鼻窦炎与鼻息肉的疗效。方法:选取350例鼻窦炎与鼻息肉患者,按随机数字表法分为两组,对照组(164例)给予综合疗法,观察组(186例)给予功能性鼻内窥镜手术联合综合疗法。通过观察并记录疗效,治疗前,治疗后3个月患者体内IL-1,IL-8水平,SF-36量表评分,评价功能性鼻内窥镜手术治疗鼻窦炎与鼻息肉的疗效。结果:经手术和药物治疗,观察组有效率明显高于对照组(P0.05),治疗前,两组IL-1和IL-8水平无统计学差异(P0.05),治疗后3个月,两组IL-1和IL-8水平均明显下降,且观察组IL-1和IL-8水平低于对照组(P0.05),治疗前,两组SF-36各项评分无统计学差异,治疗后3个月,两组SF-36评分均明显增加(P0.05)。观察组在躯体疼痛和总体健康2项评分明显高于对照组(P0.05),其余6项评分相比无统计学差异(P0.05)。结论:功能性鼻内窥镜手术对鼻窦炎与鼻息肉具有较好的疗效,能显著减轻炎症反应,改善患者生活质量,值得临床推广使用。     

鼻内镜术与鼻息肉摘除术对鼻窦炎合并鼻息肉患者的鼻腔通气功能、嗅觉功能和生活质量的影响

目的:探讨鼻内镜术与鼻息肉摘除术对鼻窦炎合并鼻息肉患者的鼻腔通气功能、嗅觉功能和生活质量的影响。方法:选取2016年1月-2017年8月期间我院收治的94例鼻窦炎合并鼻息肉患者。根据数表法将患者随机分为对照组(n=47)与研究组(n=47),其中对照组患者行传统鼻息肉摘除术,研究组则行鼻内镜术。观察两组患者临床疗效、临床指标及并发症发生情况,比较两组患者术前、术后6个月鼻腔通气功能、嗅觉功能和生活质量评分。结果:研究组临床总有效率为91.49%(43/47),高于对照组的65.96%(31/47)(P0.05)。研究组患者手术时间、术后住院时间、术中出血量均低于对照组(P0.05)。两组患者术后6个月鼻腔通气功能、嗅觉功能评分均较术前降低,且研究组低于对照组(P0.05)。两组患者术后6个月躯体功能(PF)、躯体角色(RP)、躯体疼痛(BP)、总体健康(GH)、情感角色(RE)以及心理健康(MH)均较术前升高,且研究组高于对照组(P0.05)。研究组头晕、头痛、流脓涕、鼻塞、复发等并发症发生率均低于对照组(P0.05)。结论:鼻窦炎合并鼻息肉患者采用鼻内镜术治疗,疗效确切,可显著改善患者临床指标、生活质量,对患者鼻腔通气功能、嗅觉功能均有促进作用,且术后并发症少,值得临床推广。     

Alteration of mitochondrial DNA sequence and copy number in nasal polyp tissue

This study was designed to investigate the possibility that mtDNA mutations might arise in inflammatory or chronically damaged nasal polyp tissue from 23 patients. Thirteen patients (57%) displayed nasal polyp tissue-specific mtDNA mutations in the hypervariable segment of the control region and cytochrome b gene, which were not found in the corresponding blood cells and/or adjacent normal tissue. Nasal polyp tissue-specific length heteroplasmic mutations were also detected in nucleotide position (np) 303–315 homopolymeric poly C track (39%), np 514–523 CA repeats (17%) and np 16184–16193 poly C track (30%). The average mtDNA copy number was about three times higher in nasal polyp tissue than in the corresponding peripheral blood cells and adjacent non-polyp tissues. The level of reactive oxygen species (ROS) was significantly higher in the nasal polyp tissues compared to those from the corresponding samples. High level of ROS in nasal polyp tissue may contribute to development of mtDNA mutations, which may play a crucial role in the vicious cycle of pathophysiology of nasal polyps.     

Histamine H4 receptor expression is elevated in human nasal polyp tissue

Altered histamine metabolism is thought to be involved in the pathomechanism of nasal polyposis characterized by local eosinophil infiltration. The present study was performed to determine whether histamine receptors play a role in the effect of histamine in nasal polyp tissue. The findings suggest that the expression of H1 and H4 receptors is elevated in polyp tissue (p=0.045; p<0.001), while the level of H2 and H3 receptors is not increased significantly. The elevation of H1 and H4 receptors' expression may indicate that the histamine related mechanisms are preferentially mediated through H1 and H4 histamine receptors in the polyp tissue. Simultaneously with increased H4 receptor expression, the concentration of eosinophil cationic protein (ECP) was increased significantly in polyp tissue (p=0.002). One may speculate that the H4 receptor mediated histamine effects have a role in eosinophil accumulation and activation in inflammatory diseases of the nasal and paranasal sinus mucosa, such as nasal polyposis.     

Q192R polymorphism in the PON1 gene and nasal polyp in a Turkish population

The pathogenesis of nasal polyps is not completely understood. Oxidative damage contributes to polyp formation in the nasal mucosa. The paraoxonase 1 (PON1) enzyme is an important liver enzyme with high antioxidant activity. In this study, we investigated the correlation between Q192R genotypic polymorphism of the PON1 enzyme and nasal‐polyp disease. The study examined 62 nasal‐polyp patients and 88 controls. PON1 Q192R polymorphism was determined using polymerase chain reaction‐restriction fragment length polymorphism. The genotype distribution of the PON1 gene was significantly different between nasal‐polyp patients (QQ = 69.35%, QR = 25.81%, RR = 4.83%) and healthy controls (QQ = 52.27%, QR = 44.31%, RR = 3.40%). Our results suggest that the PON1 QQ genotype (odds ratio [OR] = 2.066, P = .036) is associated with a higher risk of developing the nasal‐polyp disease while QR genotype (OR = 0.437, P = .021) showed a lower risk.     

Enhanced susceptibility of nasal polyp tissues to avian and human influenza viruses

Background

Influenza viruses bind and infect respiratory epithelial cells through sialic acid on cell surface. Differential preference to sialic acid types contributes to host- and tissue-tropism of avian and seasonal influenza viruses. Although the highly pathogenic avian influenza virus H5N1 can infect and cause severe diseases in humans, it is not efficient in infecting human upper respiratory tract. This is because of the scarcity of its receptor, α2,3-linked sialic acid, in human upper airway. Expression of sialic acid can be influenced by various factors including inflammatory process. Allergic rhinitis and nasal polyp are common inflammatory conditions of nasal mucosa and may affect expression of the sialic acid and susceptibility to influenza infection.

Methodology/Principal Finding

To test this hypothesis, we detected α2,3- and α2,6-linked sialic acid in human nasal polyp and normal nasal mucosal tissues by lectin staining and infected explants of those tissues with avian influenza viruses H5N1 and seasonal influenza viruses. We show here that mucosal surface of nasal polyp expressed higher level of α2,3- and α2,6-linked sialic acid than normal nasal mucosa. Accordingly, both H5N1 avian influenza viruses and seasonal influenza viruses replicated more efficiently in nasal polyp tissues explants.

Conclusions/Significance

Our data suggest a role of nasal inflammatory conditions in susceptibility to influenza infection, especially by avian influenza viruses, which is generally inefficient in infecting human upper airway. The increased receptor expression may contribute to increased susceptibility in some individuals. This may contribute to the gradual adaptation of the virus to human population.     

Pai syndrome: first patient with agenesis of the corpus callosum and literature review

BACKGROUND: Pai syndrome (PS) is a rare regional developmental defect of the face, mainly characterized by the variable association of midline cleft of the upper lip (MCL), duplicated maxillary median frenulum, and midline facial cutaneous and midanterior alveolar process polyps. Its entire clinical spectrum is still poorly delineated and the etiology remains unknown. CASE: We describe a 1-month-old boy presenting with MCL, left nostril hamartomatous mass, midline pedunculated polyp originating from the columella base, midline alveolar cleft, duplication of the upper median frenulum, unilateral persistent papillary membrane, lipoma of the corpus callosum, and additional minor facial dysmorphism. This patient also presents with agenesis of the corpus callosum, which has never been reported in PS. Literature review was carried out comparing clinical data of the 20 previously published patients with those observed in the present case. CONCLUSIONS: The minimum diagnostic criteria for PS has been fixed in one or more hamartomatous nasal polyps plus MCL (with or without cleft alveolus) and/or midanterior alveolar process congenital polyp. Additional common ancillary findings include duplicated median maxillary frenulum, hypertelorism, nasal cleft, midfrontal skin tags, and ocular and CNS structural abnormalities. However, mental retardation is only an occasional feature and seems to be related to coexisting conditions (such as chromosome imbalance). Literature review shows that PS is etiologically heterogeneous, as it may result from chromosome abnormalities and environmental/stochastic events, as well as de novo mutations.     

Deprived TLR9 Expression in Apparently Healthy Nasal Mucosa Might Trigger Polyp-Growth in Chronic Rhinosinusitis Patients

Background

The origin of nasal polyps in chronic rhinosinusitis is unknown, but the role of viral infections in polyp growth is clinically well established. Toll-like receptors (TLRs) have recently emerged as key players in our local airway defense against microbes. Among these, TLR9 has gained special interest in viral diseases. Many studies on chronic rhinosinusitis with nasal polyps (CRSwNP) compare polyp tissue with nasal mucosa from polyp-free individuals. Knowledge about changes in the turbinate tissue bordering the polyp tissue is limited.

Objectives

To analyse the role of TLR9 mediated microbial defense in tissue bordering the polyp.

Methods

Nasal polyps and turbinate tissue from 11 patients with CRSwNP and turbinate tissue from 11 healthy controls in total were used. Five biopsies from either group were analysed immediately with flow cytometry regarding receptor expression and 6 biopsies were used for in vitro stimulation with a TLR9 agonist, CpG. Cytokine release was analysed using Luminex. Eight patients with CRSwNP in total were intranasally challenged with CpG/placebo 24 hours before surgery and the biopsies were collected and analysed as above.

Results

TLR9 expression was detected on turbinate epithelial cells from healthy controls and polyp epithelial cells from patients, whereas TLR9 was absent in turbinate epithelial cells from patients. CpG stimulation increased the percentage cells expressing TLR9 and decreased percentage cells expressing VEGFR2 in turbinate tissue from patients. After CpG stimulation the elevated levels of IL-6, G-CSF and MIP-1β in the turbinate tissue from patients were reduced towards the levels demonstrated in healthy controls.

Conclusion

Defects in the TLR9 mediated microbial defense in the mucosa adjacent to the anatomic origin of the polyp might explain virus induced polyp growth. CpG stimulation decreased VEGFR2, suggesting a role for CpG in polyp formation. The focus on turbinate tissue in patients with CRSwNP opens new perspectives in CRSwNP-research.     

Hematic infiltrates and the expression of HLA-DR antigens in naso-sinusoidal polyps of the fibrous type

In this study fibrous nasal polyps, obtained from four patients, were analyzed by means of immunocytochemical methods for the presence of interstitial hematic cell infiltrate and HLA-DR molecule expression. This histologic type accounted for 36.4% of nasal polyps studied. Our results demonstrated that cells belonging to monocyte-macrophage lineage were mainly detected within fibrous and edematous zones (greater than 50%), whereas T cells were found within the subepithelial peripheral connective tissue (greater than 60%). Surface and gland epithelial cells appeared to be more intensely stained for HLA-DR molecules than nasal epithelium of normal subjects, thus indicating that the intensity of HLA-DR molecule expression correlated with the presence of a hematic cell infiltrate. Nasal polyps are a frequent pathology whose etiology has not yet been completely clarified. The present study provides additional information about the fibrous polyp structure and can support some speculations on the nasal polyp etiology.     

Partial purification and characterization of the tissue plasminogen activator in nasal mucosa and nasal polyp

Tissue plasminogen activator was partially purified from the inferior turbinate and nasal polyp, and its biochemical properties were investigated. Similar TPA peak positions were seen in the gel filtration chromatography of both tissues, and the molecular weight was approximately 65,000, which was comparable to TPA of pig heart (55,000-60,000). Activity of TPA from inferior turbinate was higher than that from nasal polyp. TPA from both tissues was completely inhibited by trans-aminomethyl cyclohexane carboxylic acid, dithiothreitol, and diisopropylfluorophosphate and had similar inhibition profiles to TPA from pig heart. All these findings indicate that TPA from both tissues is undoubtedly a plasminogen-activating enzyme and serine-type protease and would be biochemically identical.     

Pathophysiological classification of chronic rhinosinusitis

Background

Recent consensus statements demonstrate the breadth of the chronic rhinosinusitis (CRS) differential diagnosis. However, the classification and mechanisms of different CRS phenotypes remains problematic.

Method

Statistical patterns of subjective and objective findings were assessed by retrospective chart review.

Results

CRS patients were readily divided into those with (50/99) and without (49/99) polyposis. Aspirin sensitivity was limited to 17/50 polyp subjects. They had peripheral blood eosinophilia and small airways obstruction. Allergy skin tests were positive in 71% of the remaining polyp subjects. IgE was<10 IU/ml in 8/38 polyp and 20/45 nonpolyp subjects (p = 0.015, Fisher''s Exact test). CT scans of the CRS without polyp group showed sinus mucosal thickening (probable glandular hypertrophy) in 28/49, and nasal osteomeatal disease in 21/49. Immunoglobulin isotype deficiencies were more prevalent in nonpolyp than polyp subjects (p < 0.05).

Conclusion

CRS subjects were retrospectively classified in to 4 categories using the algorithm of (1) polyp vs. nonpolyp disease, (2) aspirin sensitivity in polyposis, and (3) sinus mucosal thickening vs. nasal osteomeatal disease (CT scan extent of disease) for nonpolypoid subjects. We propose that the pathogenic mechanisms responsible for polyposis, aspirin sensitivity, humoral immunodeficiency, glandular hypertrophy, eosinophilia and atopy are primary mechanisms underlying these CRS phenotypes. The influence of microbial disease and other factors remain to be examined in this framework. We predict that future clinical studies and treatment decisions will be more logical when these interactive disease mechanisms are used to stratify CRS patients.     

Reduced expression of activin A in focal lymphoid agglomerates within nasal polyps.

It has been previously reported that activin A, a homodimer of the betaA inhibin subunit, is secreted by stromal cells from mouse bone marrow and causes apoptotic death of mouse plasmacytoma tumor cells. Recent in vitro studies have also implicated this cytokine in the suppression of normal B-cell lymphopoiesis. In this study we examined the occurrence of activin A in nasal polyp tissues that present a combination of epithelium, mesenchyme, and vascular endothelium, with frequent massive hemopoietic infiltration. Anti-betaA-chain antibodies strongly stained epithelial mucous glands and some endothelial cells, and diffusely stained the polyp stroma. Normal adult conchae were similarly stained, whereas activin A was not detected prenatally by immunostaining of nasal tissues. Staining specificity was substantiated by ligand competition assays. Detailed examination of the inflammatory polyp infiltrate showed that activin A staining was reduced in sites of focal infiltration of B-lymphoid cells. It is therefore implied that local accumulation of a large number of B-cells is associated with relatively low activin A expression.