PDF(Pubmed)
Abstract：
UNASSIGNED: Adenoid tissue is a first-line host defense secondary lymphoid organ, especially in childhood. The endoplasmic reticulum (ER) is required to maintain balanced cellular activity. With impaired ER functions, protein accumulation occurs, resulting in ER stress, which plays a role in the etiopathogenesis of many diseases.
UNASSIGNED: We aimed to investigate the relationship between ER stress and adenoid tissue disorders, thereby elucidating the mechanisms of immunity-related diseases.
UNASSIGNED: Fifty-four pediatric patients (>3 years old) who underwent adenoidectomy for chronic adenoiditis (CA) or adenoid hypertrophy (AH) were enrolled in this prospective, parallel-group clinical study. Adenoids were divided into two groups (CA or AH) based on their size and evaluated for ER stress pathway and apoptosis pathway markers by Real-time PCR and Western blot analysis.
UNASSIGNED: ER stress pathway markers significantly differed between the CA and AH groups. Children with CA had higher ER stress marker levels than the AH group (p < .001 for ATF-4, ATF-6, and GRP78, and p < .05 for EDEM1, CHOP, EIF2AK3, ERNI, and GRP94). Apoptosis pathway marker levels (BAX and BCL-2) were not different between groups.
UNASSIGNED: ER stress contributes to the etiopathogenesis of adenoid tissue diseases and the pathogenesis of adenoid tissue disorders, which are part of the immune response. These results may guide the development of new and alternative treatments for immune system disorders.
Adenoid tissue is a first‐line host defense secondary lymphoid organ, especially in childhood. The endoplasmic reticulum (ER) is required to maintain balanced cellular activity. With impaired ER functions, protein accumulation occurs, resulting in ER stress, which plays a role in the etiopathogenesis of many diseases. We investigated the relationship between ER stress and adenoid tissue disorders. ER stress contributes to the etiopathogenesis of adenoid tissue diseases and the pathogenesis of adenoid tissue disorders, which are part of the immune response. These results may guide the development of new and alternative treatments for immune system disorders.
UNASSIGNED: We aimed to investigate the relationship between ER stress and adenoid tissue disorders, thereby elucidating the mechanisms of immunity-related diseases.
UNASSIGNED: Fifty-four pediatric patients (>3 years old) who underwent adenoidectomy for chronic adenoiditis (CA) or adenoid hypertrophy (AH) were enrolled in this prospective, parallel-group clinical study. Adenoids were divided into two groups (CA or AH) based on their size and evaluated for ER stress pathway and apoptosis pathway markers by Real-time PCR and Western blot analysis.
UNASSIGNED: ER stress pathway markers significantly differed between the CA and AH groups. Children with CA had higher ER stress marker levels than the AH group (p < .001 for ATF-4, ATF-6, and GRP78, and p < .05 for EDEM1, CHOP, EIF2AK3, ERNI, and GRP94). Apoptosis pathway marker levels (BAX and BCL-2) were not different between groups.
UNASSIGNED: ER stress contributes to the etiopathogenesis of adenoid tissue diseases and the pathogenesis of adenoid tissue disorders, which are part of the immune response. These results may guide the development of new and alternative treatments for immune system disorders.
Adenoid tissue is a first‐line host defense secondary lymphoid organ, especially in childhood. The endoplasmic reticulum (ER) is required to maintain balanced cellular activity. With impaired ER functions, protein accumulation occurs, resulting in ER stress, which plays a role in the etiopathogenesis of many diseases. We investigated the relationship between ER stress and adenoid tissue disorders. ER stress contributes to the etiopathogenesis of adenoid tissue diseases and the pathogenesis of adenoid tissue disorders, which are part of the immune response. These results may guide the development of new and alternative treatments for immune system disorders.
摘要：
■腺样组织是一线宿主防御的次级淋巴器官，尤其是在童年。维持平衡的细胞活性需要内质网(ER)。ER功能受损，发生蛋白质积累，导致ER压力，在许多疾病的病因中起作用。
■我们的目的是研究内质网应激与腺样体疾病之间的关系，从而阐明免疫相关疾病的机制。
■54例（>3岁）因慢性腺样体炎（CA）或腺样体肥大（AH）而接受腺样体切除术的儿科患者被纳入本前瞻性研究，平行组临床研究。根据腺样体的大小将其分为两组（CA或AH），并通过实时PCR和蛋白质印迹分析评估ER应激途径和凋亡途径标志物。
■ER应激途径标志物在CA和AH组之间存在显着差异。CA患儿的ER应激标志物水平高于AH组（ATF-4，ATF-6和GRP78的p<.001，而EDEM1，CHOP的p<.05，EIF2AK3,ERNI,和GRP94）。凋亡途径标志物水平(BAX和BCL-2)在组间没有差异。
■内质网应激有助于腺样体组织疾病的发病机制和腺样体疾病的发病机制，这是免疫反应的一部分。这些结果可能指导免疫系统疾病的新的和替代的治疗方法的发展。
腺样组织是一线宿主防御的次级淋巴器官，尤其是在童年。维持平衡的细胞活性需要内质网(ER)。ER功能受损，发生蛋白质积累，导致ER压力，在许多疾病的病因中起作用。我们调查了内质网应激与腺样体组织疾病之间的关系。内质网应激有助于腺样体疾病的发病机制和腺样体疾病的发病机制,这是免疫反应的一部分。这些结果可能指导免疫系统疾病的新的和替代的治疗方法的发展。
■我们的目的是研究内质网应激与腺样体疾病之间的关系，从而阐明免疫相关疾病的机制。
■54例（>3岁）因慢性腺样体炎（CA）或腺样体肥大（AH）而接受腺样体切除术的儿科患者被纳入本前瞻性研究，平行组临床研究。根据腺样体的大小将其分为两组（CA或AH），并通过实时PCR和蛋白质印迹分析评估ER应激途径和凋亡途径标志物。
■ER应激途径标志物在CA和AH组之间存在显着差异。CA患儿的ER应激标志物水平高于AH组（ATF-4，ATF-6和GRP78的p<.001，而EDEM1，CHOP的p<.05，EIF2AK3,ERNI,和GRP94）。凋亡途径标志物水平(BAX和BCL-2)在组间没有差异。
■内质网应激有助于腺样体组织疾病的发病机制和腺样体疾病的发病机制，这是免疫反应的一部分。这些结果可能指导免疫系统疾病的新的和替代的治疗方法的发展。
腺样组织是一线宿主防御的次级淋巴器官，尤其是在童年。维持平衡的细胞活性需要内质网(ER)。ER功能受损，发生蛋白质积累，导致ER压力，在许多疾病的病因中起作用。我们调查了内质网应激与腺样体组织疾病之间的关系。内质网应激有助于腺样体疾病的发病机制和腺样体疾病的发病机制,这是免疫反应的一部分。这些结果可能指导免疫系统疾病的新的和替代的治疗方法的发展。
