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Objective: To investigate the molecular mechanisms of chronic rhinosinusitis (CRS), to identify key cell subgroups and genes, to construct effective diagnostic models, and to screen for potential therapeutic drugs. Methods: Key cell subgroups in CRS were identified through single-cell transcriptomic sequencing data. Essential genes associated with CRS were selected and diagnostic models were constructed by hdWGCNA (high dimensional weighted gene co-expression network analysis) and various machine learning algorithms. Causal inference analysis was performed using Mendelian randomization and colocalization analysis. Potential therapeutic drugs were identified using molecular docking technology, and the results of bioinformatics analysis were validated by immunofluorescence staining. Graphpad Prism, R, Python, and Adobe Illustrator software were used for data and image processing. Results: An increased proportion of basal and suprabasal cells was observed in CRS, especially in eosinophilic CRS with nasal polyps (ECRSwNP), with P =0.001. hdWGCNA revealed that the "yellow module" was closely related to basal and suprabasal cells in CRS. Univariate logistic regression and LASSO algorithm selected 13 key genes ( CTSC , LAMB3 , CYP2S1 , TRPV4 , ARHGAP21 , PTHLH , CDH26 , MRPS6 , TENM4 , FAM110C , NCKAP5 , SAMD3 , and PTCHD4 ). Based on these 13 genes, an effective CRS diagnostic model was developed using various machine learning algorithms (AUC=0.958). Mendelian randomization analysis indicated a causal relationship between CTSC and CRS (inverse variance weighted: OR=1.06, P =0.006), and colocalization analysis confirmed shared genetic variants between CTSC and CRS (PPH4/PPH3>2). Molecular docking results showed that acetaminophen binded well with CTSC (binding energy:-5.638 kcal/mol). Immunofluorescence staining experiments indicated an increase in CTSC + cells in CRS. Conclusion: This study integrates various bioinformatics methods to identify key cell types and genes in CRS, constructs an effective diagnostic model, underscores the critical role of the CTSC gene in CRS pathogenesis, and provides new targets for the treatment of CRS.

Objective: To investigate the correlation between FCER2（2206A>G） gene polymorphism and the efficacy of inhaled corticosteroids（ICS） in patients with chronic rhinosinusitis（CRS）. Methods: A total of 208 CRS patients were routinely treated with functional endonasal sinus surgery and postoperative ICS. DNA extraction, PCR amplification and gene sequencing were performed to observe the FCER2（2206A>G） gene polymorphism and calculate the allele frequency. The visual analog scale（VAS） score, Lund-Kennedy score, and computed tomography（CT） Lund-Mackay score were determined 6 months after surgery among patients with different genotypes. Moreover, the polymorphism frequency was compared among different subgroups（chronic rhinosinusitis with nasal polyps versus chronic rhinosinusitis without nasal polyps, eosinophilic chronic rhinosinusitis versus non-eosinophilic chronic rhinosinusitis）. Results: There were FCER2（2206A>G） gene polymorphism in patients with CRS, and the phenotypes included 3 genotypes, AA, AG and GG, with distribution frequencies of 68（32.7%）, 116（55.8%） and 24（11.5%） cases, respectively. No significant differences were found in age, VAS score, nasal endoscopic Lund-Kennedy score and CT imaging Lund-Mackay score among patients with CRS of each genotype before surgery. In patients with the AA genotype, the changes in VAS score（5.74±1.10）, Lund Kennedy score（5.92 ± 1.14）, and CT imaging Lund-Mackay score（13.26±4.26） were significantly higher than in patients with the AG（4.37±0.86, 5.37±1.24, 10.82±3.77） and GG（4.26±0.80, 5.18±1.56, 10.10±3.53） genotype（ P <0.05）. However, there were no marked difference between patients with the AG genotype and those with the GG genotype（ P >0.05）. Compared with patients with non-eosinophilic sinusitis, Among them, the differences between the GG genotype and AG /AA genes were more significant in eosinophilic sinusitis compared to non-eosinophilic sinusitis（ P <0.01）. Conclusion: The FCER2（2206A>G） gene in patients with CRS has genetic polymorphism and is associated with the recovery of CRS patients after surgery, individual corticosteroid sensitivity, and subgroup variability., Competing Interests: The authors of this article and the planning committee members and staff have no relevant financial relationships with commercial interests to disclose., (Copyright© by the Editorial Department of Journal of Clinical Otorhinolaryngology Head and Neck Surgery.)

Objective: To identify the differentially expressed genes in nasal epithelial cells from chronic rhinosinusitis with nasal polyps (CRSwNP), and to analyze related genes which are involved in deficiency of nasal epithelial barrier in CRSwNP patients by analyzing the datasets download from the gene expression omnibus(GEO) database. Methods: The mRNA expression microarray data numbered GSE107624 (7 CRSwNP and 7 controls) and GSE69093 (13 CRSwNP and 11 controls) were downloaded from the publicly available GEO database. These two datasets were jointly analyzed to screen the differentially expressed genes in nasal epithelial cells of controls and CRSwNP patients. In the meanwhile, we further evaluated the function annotation and regulatory pathways of the differentially expressed genes. To further confirmed what we have observed, sinus tissues were collected from patients with CRSwNP (14 cases, 46.8±17.9 years) and uncinate process tissues were collected from patients with nasal septum deviation (7 cases, 23.4±2.3 years) as control group. The primary epithelial cells of nasal mucosa were cultured and the mRNA level of screened genes were measured by Q-PCR. SPSS 22.0 software was used to for statistical analysis. Results: GSE107624 dataset showed that there were 3 856 differentially genes in nasal epithelial cells between CRSwNP and control group, while there were 771 differentially expressed genes in GSE69093 dataset. Finally, 55 up-regulated genes and 3 down-regulated genes were noticed in nasal epithelial cells of CRSwNP patients in the two datasets. GO gene functional annotation analysis showed that SPTBN1 , FNBP1L , VAPB and SNX1 were involved in cell adhesion function, MAP1B was participated in the formation of microtubule related complex. KEGG pathway enrichment analysis indicated that BAMBI and SIAH1 were involved in regulation of Wnt pathway, COL6A1 and EIF4E were involved in the regulation of PI3K-AKT pathway. String protein interaction network analysis assumed that MAP1B and VAPB were the core functional proteins. Among top 3 differentially expressed genes COL6A1 , MAP1B and BAMBI , only MAP1B gene was increased in nasal epithelial cells of CRSwNP patients in comparison to controls. Conclusion: The increased MAP1B gene in epithelial cells of CRSwNP, as well as abnormal regulation of Wnt and PI3K-AKT signal pathways may mediate the barrier dysfunction in CRSwNP.

Objective: To investigate the expression and clinical significance of TET gene and 5hmC in chronic sinusitis. Methods: Acquiring 20 cases of nasal polyps from chronic sinusitis with polyps（CW）, 20 cases of uncinate process tissues from chronic sinusitis without polyps（CS）, 10 cases of middle turbinate tissues from patients with nasal septum deviated as normal group（N）.The expression of TET gene and 5hmC in chronic sinusitis was measured by immunofluorescence, Western-Blot and Quantitative real-time PCR. Results: Both TET1/2/3 gene and 5 hmC were highly expressed in the CS group, but were lower in the CW group and the N group.There were statistically significant differences between the CS group and the CW group（ P <0.05）, and between the CS group and the N group（ P <0.05）.The expressions of TET1 and TET3 in the N group were higher than those in the CW group, and the difference was statistically significant（ P <0.05）. Conclusion: DNA demethylation plays an important role in the formation of nasal polyps.High expression of TET1, TET2, TET3 and 5hmC May reduce the risk of nasal polyps.Increased DNA demethylation in chronic sinusitis may reduce the risk of nasal polyp formation.When the degree of DNA methylation in chronic sinusitis is high and the degree of DNA demethylation is low, the disease may develop to CRSwNP, and when the degree of DNA methylation is low and the degree of DNA demethylation is high, the disease may develop to CRSsNP., Competing Interests: The authors of this article and the planning committee members and staff have no relevant financial relationships with commercial interests to disclose., (Copyright© by the Editorial Department of Journal of Clinical Otorhinolaryngology Head and Neck Surgery.)

Objective: To explore the gene promoter methylation profiles of nasal polyp, and to analysis the promoter methylation differences between the nasal polyp and the normal nasal mucosa. Method: Total DNA of the nasal polyp tissues and normal nasal mucosa were extracted. After immunoprecipitation and whole genome amplification, the DNA was labeled with Cy3/5 and hybridized in NimbleGen hybridization chamber. For array hybridization, Roche Nimblegen CpG Promoter array was used. The slides were scanned using the Axon GenePix 4000B microarray scanner. The different genes were analyzed through pathway and verified by Real-time PCR. Result: 3010 genes were found to have promoter hypermethylation in normal nasal mucosa or nasal polyp.2,62%(79/3010) of the genes had promoter hypermethylation in all the nasal polyps, which were negative in normal nasal mucosa.10.66%(321/3010) of the genes had promoter hypermethylation in normal nasal mucosa, which were negative in all the nasal polyps. Three pathways were found in the promoter hypermethylation of the nasal polyps. Fourteen pathways were found in the negative hypermethylation of the nasal polyps. Conclusion: Genes promoter methylation plays an important role in the development of nasal polyps, and the gene promoter methylation profiling may yield new some clues on the mechanism of nasal polyps., Competing Interests: The authors of this article and the planning committee members and staff have no relevant financial relationships with commercial interests to disclose., (Copyright© by the Editorial Department of Journal of Clinical Otorhinolaryngology Head and Neck Surgery.)

Objective: The aim of this study is to investigate the relationship between Filaggrin ( FLG ) gene mutations and nasal polyps. Method: Genomic DNA was extract from 48 nasal polyps tissues, and 30 samples of inferior turbinate tissues from normal human controls. Two FLG gene mutation points (R501X and 3321delA) were detected by polymerase chain reaction (PCR) first, then detected by polypropylene gel electrophoresis, and finally gene sequencing. Result: The FLG gene c. 3321delA was found in 2 cases (4.17%) of nasal polyps, both of them were heterozygous mutations. and the control group did not detected this mutation. At the same time, the new mutation site of FLG (c. 1711C>A) was found 12 patients in cases group (25.00%), two of which were homozygous mutation 4.17% (2/48). Only one of homozygous mutation was found in the control group 3.33% (1/30). The difference of c. 1711C>A in mutation rate between the case group and the control group was statistically significant ( P <0.05). Conclusion: The mutation of the FLG gene is associated with the occurrence and the development of nasal polyps, which may be one of the causes of nasal polyps.

Objective: To investigate the expression of autophagy-related gene Beclin1 and P62 in nasal polyps and its relationship with the pathogenesis of this disease., Methods: The specimens were divided into two groups: nasal polyp tissue(n=50) and normal inferior turbinate mucosa(n=20). The general morphology was detected with hematoxylin-eosin(HE) staining, the expression of Beclin1 and P62 was examined with immunohistochemistry(IHC) and real-time fluorescent quantitative reverse transcription-polymerase chain reaction ( RT-PCR). SPSS 20.0 software was used to analyze the data., Results: Protein level: The expression of Beclin1 in nasal polyp tissue was lower than inferior turbinate mucosa(U=-13.36, P<0.01), in contrast, P62 in experimental group was higher than control group(U=12.99 , P<0.01). mRNA level: The relative quantity of Beclin1 and LC3B expressions in nasal polyp were 0.46±0.17 and 0.46±0.11, which was lower than those in turbinate mucosa 1.11±0.47 and 0.96±0.25.The differences were significant(t value was -4.61, -4.61, both P<0.01). But the relative quantity of P62 expression in nasal polyp was 2.19±0.44, which was higher than that in turbinate mucosa (1.05±0.33). The difference was all significant(t=6.16, P<0.01)., Conclusions: Compared with control group, the expression of Beclin1 was deficient and P62 was much more. Autophagy was deficient in nasal polyps, which might be in connection with the pathogenesis of the disease.

Nasal polyps is a common disease in clinical, with nasal mucosal inflammatory hyperplasia. However, the molecular mechanism of it is largely unknown. Tumor suppressor genes, proliferation and apoptosis related genes and cytokines play an important role in the formation and pathological development of nasal polyps. The expression level of tumor suppressor related proteins and receptors is not constant, high level of these expression can stimulate nasal mucosal proliferation, while low or lacking expression may facilitate nasal polyps cells apoptosis. Both proliferation and apoptosis make a big difference in nasal polyps formation and development. This article concludes the relationships between new progressions in nasal polyps pathogenesis and tumor suppressor genes and proliferation apoptosis genes, which not only helps practitioners deeply and comprehensively understand nasall polyps pathogenesis but promotes explorations to effective therapeutics.

Objective: The expression of C/EBPα, CK10 in nasal inverted papilloma (NIP) were detected in the study. Further discussed their significance in genesia, development and recurrence of NIP., Method: Three groups including nasal cavity mucosae (NM 10 cases), nasal polyp (NP 20 cases) and NIP (30 cases) were selected in the study. Expretion of C/EBPα, CK10 were detected by immunohistochemisty PV-6000 method., Result: (1) The different expression of C/EBPα and CK10 in the group of NM, NP and NIP was statistically significant (P < 0.05). (2) The different expression of C/EBPα, CK10 in the group of benign NIP and NIP with atypical hyperplasia was statistically significant (P < 0.05). (3) The different expression of C/EBPα and CK10 in the group of NIP with recurrence and NIP with no recurrence was statistically significant, P < 0.05, respectively. (4) Our result indicate that the relationship of C/EBPα and CK10 (r = 0.578, P < 0.01) was direct correlation. The difference was statistically significant., Conclusion: In conclusion, the present results describe C/EBPα, CK10 expression in NIP and their possible implication in the regulation of tumor growth and differentiation. C/EBPα and CK10 production may prove useful in terms of a prognostic marker for the recurrence in nasal inverted papilloma.

Objective: To investigate the relationship between the promoter polymorphism of IL-4 and IL-6 and chronic rhinosinusitis (CRS)., Methods: One hundred and twenty-three patients with CRS and 239 healthy controls in Shanghai region were chosen in this study. The genotype of IL-4 gene -33T>C and -590C>T were determined using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method and the genotype of IL-10 gene -1082A>G was determined using amplification refractory mutation system-polymerase chain reaction (ARMS-PCR) method. Statistical calculations were performed using SAS 8.2 software., Results: Significant differences were found in genotype distribution of -33T>C and -590C>T between the CRS group and the control group (χ2=6.6013, P=0.0102, χ2=6.6013, P=0.0304), and -33T>C remained significant following application of the Bonferroni correction (P<0.025). The relative risks of CRS with -33T>C and -590C>T were 1.818(P=0.0236, 95%CI 1.084-3.050) and 1.838 (P=0.0147, 95%CI 1.127-2.997). There was linkage disequilibrium (LD) between the -33T>C and -590C>T. The coefficient of linkage disequilibrium (D') was 0.77 and the related coefficient (r2) was 0.54. The -33T/-590T haplotype was associated with CRS and the relative risk was 1.653 (P=0.0130, 95%CI 1.107-2.469). There were only two genotypes of IL-10 gene-1082A>G and the frequencies of the AA and AG genotypes were not different between the CRS and control groups., Conclusion: The promoter polymorphism of IL-4 -33T>C and -590C>T were associated with the susceptibility of CRS and the -33T/-590T haplotype was a risk factor for CRS, but there were no association between the -1082A>G and CRS.

Objective: Chronic rhinosinusitis was often exacerbated by viral infection. A disruption of the mechanisms that regulate the activity of matrix metalloproteinases (MMPs) during viral infection was one possible mechanism responsible for the exacerbation. The purpose of study was to achieve a better understanding of MMP expression in nasal epithelial cells after viral infection., Methods: Human nasal epithelial cells were isolated from nasal polyp specimens obtained during endoscopic endonasal surgery in chronic rhinosinusitis patients. The expression of MMP-2, MMP-9, and tissue inhibitor of metalloproteinase (TIMP)-1 mRNA in primary human nasal polyp epithelial cells after double stranded RNA (ds RNA) stimulation were investigated., Results: Among the genes whose expression was evaluated, only expression of MMP-9 mRNA increased significantly after dsRNA stimulation (22.61 +/- 5.47 fold increase, Z = -2.52, P = 0.012)., Conclusions: The significant up-regulation of MMP-9 mRNA, which was not modulated by TIMP-1, was an additional source of increased proteolytic activity in virus-infected upper airways that might contribute to the exacerbation of chronic rhinosinusitis with nasal polyps.

Objective: To investigate the expression of Toll-like receptors (TLRs) signaling pathway in chronic rhinosinusitis (CRS) with nasal polyps., Method: Gene microarray analysis was used to detect the expression of TLRs signaling pathway in CRS with nasal polyps., Result: Of 19 differentially expressed (two fold changes), 4 genes were upregulated and 15 genes were downregulated., Conclusion: The differentially expressed genes in TLRs signaling pathway may exert its effect in the pathogenesis of CRS. In addition, the roles of TLR9 and its agonists need further study.

Objective: To detect the mucin gene (MUC2, MUC5AC, MUC5B, MUC18 and MUC19) expression in the nasal polyps, allergic rhinitis (AR) and the normal nasal mucosa in human. To investigate the role and clinical significance of mucin gene in the pathogenesis of nasal polyps and AR patients., Method: We obtained samples from 35 cases of nasal polyps, 18 cases of AR inferior turbinate and 18 cases of simple nasal septum deviation inferior turbinate. Specimens were analyzed with RT-PCR and Real-time FQ-RT-PCR., Result: The results of RT-PCR and FQ-RT-PCR showed that the expression of MUC5AC, MUC5B in nasal polyps and AR patients was significantly higher than that in normal mucosa (P<0.05). The expression of MUC5AC, MUC5B in nasal polyps was not significantly different from that in AR patients (P>0.05). The expression of MUC2, MUC18 in nasal polyps and AR was not significantly different from that in normal mucosa (P>0.05). And the results of RT-PCR for MUC19 expression in AR was higher than that in nasal polyps group and normal group (P<0.05 or P<0.01)., Conclusion: MUC5AC and MUC5B are highly expressed in epithelium of human nasal polyps and AR, and they take part in mucus over-secretion in nasal polyps and AR. The expression of MUC19 in AR was higher than that in nasal polyps group and normal group. It indicates that the secretion of MUC19 in allergic rhinitis was on high level. There was no difference of the expression of MUC2 and MUC18 in nasal polyps group, AR group and in normal group.

Objective: To explore the changes in gene expressions in the human nasal polyp., Method: A 14500 gerie DNA microarray (Affymetrix) was used to examine gene expressions in 6 NP samples, 6 normal mucosal samples. The differentially expressed genes were identified and subjected to realtime PCR analysis., Results: The differentially expressed genes mostly involved in cytokines, adhesion genes about complements and their receptors, immune transcription regulatory molecules, signal transduction, differentially expressed genes including IL-8, RGS1, GRK4, CCL20, uteroglobin. The results of IL-8, RGS1 Real-time PCR of were consistent with that of gene chip analysis., Conclusion: Microarray expression profile of NP samples is differential. RGS1 may play an important role in cell signal transduction, IL-8 may involve in occurrence of nasal polyps by inducing cells releasing inflammatory factors.

Objective: To investigate the gene expression profile by using gene chip technology and probe into the role of corresponding gene in the pathogenesis of nasal polyps by analysing the difference of the gene depression., Method: The total RNAs were respectively extracted from 6 pairs of inferior turbinates and nasal polyps, and then were reversely transcribed to cDNAs with incorporation of fluorescent dUTP as the hybridization probes. The mixed probes were then hybridized with the BiostarH-40 s gene chips, it was scanned by laser scanner and the acquired image was analyzed by software., Result: 1887 genes were differently expressed in gene profile of nasal polyps, among which 1099 were upregulated and 788 were down-regulated. Six genes were found in all gene chips, among which 4 genes were upregulated and 2 were down-regulated. The 6 genes encoded the protein of the transmembrane 4 superfamily, highly similar to GAMMA-interferon-inducible protein IP-30 precursor, highly similar to complement factor I precursor and insulin-like growth factor binding protein 3 (IGFBP3)., Conclusion: Detecting the differently expressed genes will provide clues and theoretical foundation for the pathogenesis of nasal polyps. The nasal polyps is a polygenic disease and the genes of GAMMA-interferon-inducible protein, insulin-like growth factor binding protein may play an important role in its pathogenesis.

Objective: To investigate the genetic mode of nasal polyp and the effect of genetic factor on occurrence of the disease., Methods: A genetic epidemiological case-control study including 280 pedigrees (120 nasal polyp cases and 160 controls) was conducted. The segregation ratio and the heritability of nasal polyp were respectively estimated by the Li-Mantel-Gart method and the Falconer method., Results: The segregation ratio was 0.124 (95% CI 0.081-0.167), significantly lower than 0.25, which showed that nasal polyp did not possess the characteristics of monogenetic model. The prevalence rate of first-degree and second-degree relatives in cases were 8.571% and 3.086% respectively, which were significantly different (X2 = 24.851, P < 0.01) and were higher than that noticed 1.376% and 1.141% in controls (X2 = 33.547 and 14.274, all P < 0.01). The heritability of the first-degree and second-degree relatives of nasal polyp was 64.488% and 61.947%. Among the first-degree relatives of nasal polyp probands, the heritability of the adult group and the children group were respectively 60.735% and 74.598% (the difference was significant, X2 = 4.504, P < 0.05). The heritability of the first-occurred group was 62.839% and the recurred group was 74.304% (the difference was significant, X2 = 4.105, P < 0.05)., Conclusions: This study indicated that the genetic model of nasal polyp belonged to polygenetic and the genetic factors played an important role in the occurrence of nasal polyp, especially for young or recurred patients.

Objective: To analyse the relationship between superantigens produced by Staphylococcus aureus and the mRNA expression of T-cell receptor V beta region (TCR Vbeta), and to investigate the possible role of Staphylococcal superantigens in the pathogenesis of nasal polyps., Methods: Sinonasal mucus and polyp/mucosa tissue were obtained from patients with chronic rhinosinusitis (22 patients with bilateral nasal polyps, 15 without nasal polyps) and 12 normal subjects as comparative negative controls. Mucus specimens were assayed by enzyme-linked immunosorbent assay (ELISA) for Staphylococcal exotoxins,and analyzed for the expression of TCR Vbeta genes using the technique of reverse transcriptase-polymerase chain reaction (RT-PCR)., Results: The percentages of Staphylococcus exotoxins in nasal polyps were 54.54% (21/22) for chronic rhinosinusitis with nasal polyp (CRSwNP) subjects. There were no positive results in the CRSsNP or control groups. The expressional intensity of Vbeta3 (10.02), Vbeta14 (3.54), Vbeta15 (2.39), Vbeta17 (3.48), and Vbeta20 (2.94) was increased significantly for Staphylococcal exotoxin B (SEB) positive subjects (P < 0.05). Vbeta2 (13.8) and Vbeta6. 1-3 (6.53) were significantly highly expressed for toxic shock syndrome toxin-1 (TSTf-1) positive subjects in CRSwNP group (P < 0.05). There were no dominantly used Vbeta fragments in ELISA- negative specimens. In the group of chronic rhinosinusitis without nasal polyp (CRSsNP), most of TCR Vbeta gene subfamilies demonstrated a trend toward higher expressional levels compared with those of normal controls, although there was no statistical difference (P > 0.05)., Conclusions: There was relationship between Staphylococcal superantigens and the excursion of TCR Vbeta gene spectra in nasal polyp, and superantigens possibly play an important role in the pathogenesis of CRSwNP.

Objective: To detect the expression of the glucocorticoid receptor-alpha (GR-alpha) mRNA in nasal polyp and normal nasal mucosa and investigate the significance of GR-alpha in progression of nasal polyp., Method: The expression of GR-alpha mRNA in 36 samples of nasal polyp and 31 samples of normal nasal mucosa was examined by using fluorescent quantitative PCR(FQ RT-PCR)., Result: The GR-alpha mRNA levels in normal nasal mucosa [(135.4 +/- 5.2) x 10(10) copy/g] were significantly higher than those in nasal polyp [(25.5 +/- 5.0) x 10(10) copy/g] (P < 0.01)., Conclusion: The low expression of GR-alpha mRNA in nasal polyp is related to the progression of nasal polyp.

Objective: To investigate the expression profile of immune associated genes in nasal polyps by gene chip technology and to probe into the role of correlative genes in the immune pathogenesis of nasal polyps., Methods: Microarray analysis was used to find the expressing profile of 491 immune associated genes in nasal polyps. The total RNAs were respectively extracted from four samples of nasal polyps and inferior turbinates, and then were reversely transcribed to cDNAs with incorporation of fluorescent dUTP as the hybridization probes. The mixed probes were then hybridized with two pieces of immune associated gene chip. It was scanned by laser scanner and the acquired image was analyzed by software., Results: Eighty-seven genes were differently expressed in immune associated gene profile of nasal polyps, among which 45 genes were upregulated and 42 genes were down regulated. Fifteen genes were shown differential expression in both chips with 5 upregulated genes and 10 downregulated genes. The differentially expressed genes mostly involved in cytokines and their receptors, chemokines and their receptors, adhesion molecules, leukocytes differential antigens, immune signal transduction molecules, and still included some genes about complements and their receptors, immune transcription regulatory molecules, innate immune molecules and neural immune molecules., Conclusions: The differently expressed genes in immune associated gene chips will provide clues and theoretical foundation for the pathogenesis of nasal polyps. Furthermore IL-17 may have an important role in the occurrence of nasal polyps, and the role of innate immunity and immune signal transduction molecules in the pathogenesis of nasal polyps need further researches.

Objective: To investigate the effect of intranasal glucosteroid treatment on the expression of interleukin (IL)-5 gene in nasal polyps., Methods: Nasal polyps from topical steroid treated patients (n = 20) and untreated patients (n = 20) were investigated with the technique of mRNA in situ hybridization., Results: The majority of IL-5 mRNA positive cells in nasal polyps were lymphocytes or eosinophils. No statistical significance was found in the densities of IL-5 mRNA positive cells between allergic patients [(12.6 +/- 4.6)/0.25mm2] and nonallergic patients [(14.3 +/- 4.1)/0.25mm2] (t = -0.775, P > 0.05). Compared with the control group [(13.9 +/- 4.2)/0.25mm2], the density of IL-5 mRNA positive cells was decreased in the steroid-treated group [(10. 2 +/- 3.1)/0.25mm2], and the difference reached statistical significance (t = 3.114, P < 0.01)., Conclusions: These findings indicate that topical steroid treatment may suppress the IL-5 gene expression, and steroids may inhibit eosinophil functions.

Objective: To look for the correlated gene of nasal polyp., Method: The nasal polyp was analysed by mRNA difference to demonstrate, and the fragment of writing was analysed and appraised., Result: The amplification products of normal conchae tissue were compared with the nasal polyp tissue under the condition of background with one accord. The total 11 difference fragments were discovered during the 150-700 bp. One of the fragments (X-1) was completely homology with the section series of the eight chromosome long arm. There was a zine finger protein in the upper stream and the down stream. The fragment expressed in nasal polyp tissue., Conclusion: Based on polymerase chain reaction (pcr), using differential display R. T. PCR (DD-RTPCR) technique, the difference express gene of nasal polyp could be effectively compared with normal nasal conchae tissue or cells, the correlated gene of nasal polyp tissue could screened out. The fragment (X-1) that was completely homology with the section series of the eight chromosome long arm may be a new identified gene which cause the nasal polyp.

Using 32P labelled rat ANF cDNA probe, the ANF gene transcripts in rat nasal mucosa and the effect of glucocorticoid and estrogen on the ANF gene transcripts was examined by Dot blot and Northern blot hybridization. Further more, the gene expression of ANF in nasal mucosa tissues of some patients with nasal diseases were also examined. The results showed that nasal mucosa contained ANF mRNA which could synthesize ANF. Both estrogen and glucocorticoid could enhance ANF gene expression in nasal mucosa with dose dependance. The gene expression of ANF in nasal polyps and inferior turbinate mucosa of patients with nasal polyps was more evident than that in other pathological conditions. The clinical significance of ANF in nasal mucosa was also discussed.