Evaluation of patients with nasal polyps about the possible association of desmosomal junctions, RORA and PDE4D gene.
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Abstract:
Nasal polyposis is chronic inflammatory disease of the nasal mucosa of the nose and sinuses, often associated with chronic non-allergic rhinitis, aspirin intolerance and non-allergic asthma. The etiology of nasal polyposis is unknown. Multiple factors contribute to the development of nasal polyps including genetic predisposition.This study was conducted on patients applied due to nasal polyps. Blood samples were collected peripheral vein and stored at 4°C until analysis for DNA extraction. Genomic DNA was extracted from peripheral blood by a standard method, samples were studied in real time PCR. All patients were evaluated about the possible association of DSG1 (rs7236477-G, 96 rxn), DSG3 (rs1941184-C, 96 rxn), PDE4D (rs1588265) and RORA (rs11071559) gene.32 patients (17 male, 15 female) with nasal polyposis were included to the study. The mean age was 34.9 ± 17.7 years, ranging between 18 and 55 years. Control group was consisted with 50 healthy volunteers without a history of nasal polyp. DSG1, DSG3 and RORA values of the study group were not statistically different from control group (p > 0.05). PDE4D values of the study group were significantly different from control group (p < 0.05).Multiple factors contribute to the pathogenesis of nasal polyps including genetic predisposition. The PDE4D family has gained interest in the complex pathogenesis of nasal polyposis. This is likely linked to the mucosal inflammatory response.Keywords:
Nasal Polyps
Pathogenesis
Etiology
Genetic predisposition
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The aim of the study was to determine whether patients with nasal polyps have a hyperreactive nasal mucosa and/or bronchi and whether there is any correlation between nasal and bronchial hyperreactivity. Twenty-six healthy volunteers and 10 consecutive patients with nasal polyps participated in the study. They were challenged with increasing concentrations of histamine. The nasal mucosa response was studied with rhinostereometry and the bronchial response was estimated by peak flow. One of the patients was mildly hyperreactive in the nose and 6 patients were hyperreactive in the bronchi. There was no correlation between nasal and bronchial hyperreactivity. Patients with nasal polyps do not have a hyperreactive nasal mucosa but there seems to be a high incidence of bronchial hyperreactivity in patients with nasal polyps.
Nasal Polyps
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Sex steroid hormone receptors (SSHR) were determined in 14 cases of sinonasal papillomas, 17 cases of nasal polyps and in the normal nasal mucosa of 13 patients. The determination of SSHR was done by the dextran-coated charcoal assay from cytosol protein. All the cases of sinonasal papilloma were SSHR negative, while some specimens of normal nasal mucosa contained small amounts of SSHR. In addition, some cases of nasal polyps were found to contain low concentrations of the receptors, but concentrations were lower than those found in normal mucosa. Although nasal papillomas are more common in men than in women, this study shows that SSHR do not play any role in the development of these tumors.
Nasal Polyps
Steroid hormone
Inverted Papilloma
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Etiology
Pathogenesis
Inflammatory Bowel Diseases
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Objective To estimate the roles of CD 43 , CD 20 and total IgE in the pathogenesis of nasal polyps. Method Twenty-six cases of nasal polyps and 20 cases of mucosa of middle turbinates were used in present study. Results The number of CD + 43 cells,CD + 20 cells and plasma cells in nasal polyps were significantly more than that in middle turbinates (P0.01). The positive rate of local IgE + cells in nasal polyps was significantly higher than in middle turbinate (P0.01). Conclusion There were active cellular immunity and humoral immunity in nasal polyps. Local allergy may play a role in the pathogenesis of nasal polyps.
Nasal Polyps
Pathogenesis
Turbinates
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Nasal polyps (NPs) are one of the most common inflammatory mass lesions of the nose, affecting up to 0.5-4% of the population. The pathogenesis of NPs has been studied widely, but it is not clearly understood. A possible role of S. aureus in nasal polyposis has been suggested by numerous studies. This study aimed to map S.aureus colonisation in NP patients in the nose in comparison to healthy controls.
Nasal Polyps
Pathogenesis
Mucous membrane
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To investigate the expression of autophagy-related gene Beclin1 and P62 in nasal polyps and its relationship with the pathogenesis of this disease.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.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).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
Pathogenesis
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Etiology
Pathogenesis
Nasal Polyps
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To explore the expression of γδ T cells in chronic rhinosinusitis (CRS) and its potential significance in pathogenesis.γδ T cell expression was detected by immunohistochemistry (Envision method). From polyps (25 CRS patients with nasal polyps, CRSwNP), inferior turbinate mucosa (13 CRS patients without nasal polyps, CRSsNP), and 16 inferior turbinate mucosa from patients with deviation of nasal septum served as control. The infiltration of eosinophils in eosinophilic CRSwNP was observed by HE staining. The differences of expression of γδ T cells between each groups were compared, meanwhile the relationship between γδ T cells and eosinophils were analyzed. SPSS 16.0 software was used to analyze the data.The positive range of γδ T cells in CRSwNP group and CRSsNP group was 88.0% and 84.6%, respectively, both higher than 37.5% in control group (χ(2) = 13.413, P < 0.01, χ(2) = 6.564, P < 0.05, respectively), CRSwNP group had no statistical significance compared with CRSsNP group (χ(2) = 0.086, P > 0.05). The expression of γδ T cells in CRSwNP group was stronger than CRSsNP group and control group (U = 596, P < 0.01, U = 296, P < 0.01, respectively); CRSsNP group was stronger than control group (U = 216, P < 0.05). There was a positive correlation between γδ T cells and eosinophils (r = 0.579, P < 0.05).The expression of γδ T cells was increased in nasal mucosa of CRS. γδ T cells may be involved in the pathogenesis of CRS.
Nasal Polyps
Pathogenesis
Chronic Rhinosinusitis
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The common factor of inflammatory bowel diseases is the unknown etiologic agent. It's suggested that it could be genetic predisposition, environment and immunologic factor. It seems probable that the etiology of these diseases has many sources but the pathogenesis is similar. Inflammatory bowel diseases etiology requires more research but the immunological system disturbances are out of the question. The most typical course of these diseases is the one with remissions and relapses. Clinical symptoms vary and depend on localization, phase and presence of complications. In this paper we present some basic information about epidemiology, pathogenesis and the clinical course of inflammatory bowel diseases.
Pathogenesis
Etiology
Inflammatory Bowel Diseases
Genetic predisposition
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Bronchopulmonary dysplasia （ BPD） is a main cause of morbidity and mortality in preterm infant,so the etiology and pathogenesis of BPD is one of the hot issues in the neonatal medical research. Present studies,not only focus on the congenital factors,including genetic susceptibility and lung immaturity,but also the acquired factors,including oxygen toxicity,barotrauma and capacity of injury,infection or inflammation. This pa-per reviews recent research progress on the etiology and pathogenesis of new pulmonary hypoplasia.
Key words:
Bronchopulmonary dysplasia; Pathogenesis; Etiology
Bronchopulmonary Dysplasia
Pathogenesis
Etiology
Genetic predisposition
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