背景:腺样体作为细菌病原体和免疫分子的储库,并且它们显著涉及患有渗出性中耳炎(OME)的儿童。作为细胞间物质传递和信号转导的重要载体,具有不同生物学功能的外泌体可以由各种类型的细胞分泌。关于外泌体与OME的临床相关性仍然存在显著的不确定性,特别是在其病理生理发展中。在这项研究中,我们将寻求确定伴有OME的腺样体肥大(AHOME)儿童外泌体的生物学功能。
方法:4-10岁儿童OME的诊断标准包括病程至少3个月,B型或C型声导纳,和不同程度的传导性听力损失。当鼻内窥镜检查显示鼻孔中至少有60%的腺样体闭塞或鼻咽侧位X线显示A/N>0.6时,可诊断为腺样体肥大。符合腺样体切除术适应症的儿童接受腺样体切除术。外周血,鼻咽拭子,从病人身上收集腺样体组织,和外泌体将从样品中分离。在最初的收集之后,患者将接受腺样体切除术,3个月后将再次收集外周血和鼻咽拭子。
结果:本研究旨在确定AHOME患儿和单纯腺样体肥大患儿术前腺样体组织和外周血样本的外泌体差异。此外,它试图确定这些群体之间腺样体组织中微生物多样性的变化。
结论:这些发现有望为OME的诊断和治疗提供新的见解,为了识别新的生物标志物,并增强我们对OME病理生理学的理解,可能导致创新诊断和治疗方法的发展。
BACKGROUND: The adenoids act as a reservoir of bacterial pathogens and immune molecules, and they are significantly involved in children with otitis media with effusion (OME). As an essential carrier of intercellular substance transfer and signal transduction, exosomes with different biological functions can be secreted by various types of cells. There remains significant uncertainty regarding the clinical relevance of exosomes to OME, especially in its pathophysiologic development. In this study, we will seek to determine the biological functions of exosomes in children with adenoid hypertrophy accompanied by OME (AHOME).
METHODS: The diagnostic criteria for OME in children aged 4-10 years include a disease duration of at least 3 months, type B or C acoustic immittance, and varying degrees of conductive hearing loss. Adenoidal hypertrophy is diagnosed when nasal endoscopy shows at least 60% adenoidal occlusion in the nostrils or when nasopharyngeal lateral X-ray shows A/N > 0.6. Children who meet the indications for
adenoidectomy surgery undergo
adenoidectomy. Peripheral blood, nasopharyngeal swab, and adenoid tissue will be collected from patients, and the exosomes will be isolated from the samples. Following the initial collection, patients will undergo
adenoidectomy and peripheral blood and nasopharyngeal swabs will be collected again after 3 months.
RESULTS: This study aims to identify differences in exosomes from preoperative adenoid tissue and peripheral blood samples between children with AHOME and those with adenoid hypertrophy alone. Additionally, it seeks to determine changes in microbial diversity in adenoid tissue between these groups.
CONCLUSIONS: The findings are expected to provide new insights into the diagnosis and treatment of OME, to identify novel biomarkers, and to enhance our understanding of the pathophysiology of OME, potentially leading to the development of innovative diagnostic and therapeutic approaches.