Necroptosis Underlies Neutrophilic Inflammation Associated with the Chronic Rhinosinusitis with Nasal Polyps (CRSwNP)

坏死性下垂 鼻息肉 上睑下垂 促炎细胞因子 免疫学 炎症 趋化因子 程序性细胞死亡 医学 嗜酸性粒细胞 肿瘤坏死因子α 细胞凋亡 病理 炎症体 生物 生物化学 哮喘
作者
Yadong Xie,Min Li,Kun Chen,Haoxiang Zhu,Mengyao Tang,Chun Zhou,Yaoming Zheng,Jing Wen,Miaomiao Han,Jia Zhang,Ke‐Qing Zhao,Hui Xiao,Huabin Li
出处
期刊:Journal of Inflammation Research [Dove Medical Press]
卷期号:Volume 14: 3969-3983 被引量:14
标识
DOI:10.2147/jir.s322875
摘要

Necroptosis is an inflammatory cell death associated with a variety of chronic diseases. Chronic rhinosinusitis with nasal polyps (CRSwNP) is a chronic inflammatory disease accompanied by eosinophil and neutrophil infiltration. The role of necroptosis in the pathogenesis of CRSwNP remains elusive.Cell death, including apoptosis, pyroptosis and necroptosis in control sinonasal mucosa and CRSwNP, were analyzed by immunoblotting, immunohistochemistry (IHC) and immunofluorescence (IF) staining for cleaved caspase 3, cleaved gasdermin D and p-MLKL, respectively. Correlations between necroptosis, inflammatory cytokines and neutrophil infiltration were assessed and a possible role of necroptosis in CRSwNP was evaluated. Primary nasal polyp cells (DNPCs) were stimulated with damage-associated molecular patterns (DAMPs) including ATP or IL-1α and their expression of inflammatory cytokines was analyzed using RT-PCR. The expression of TNF-α and IFNs in nasal polyps was measured by ELISA; human monocyte THP-1 cells were treated with TNF-α or IFN-γ and cell death was measured by LDH release.Necroptosis, rather than apoptosis or pyroptosis, was overtly activated in both eosinophilic and non-eosinophilic CRSwNP as evidenced by the presence of prominent phosphorylation of MLKL compared to controls. The abundance of DAMPs (IL-1α, HMGB1), inflammatory cytokines (IL-6) and chemokines (IL-8, CXCL-1) were all increased especially in non-eosinophilic CRSwNP. The extent of necroptosis was positively correlated with the abundance of DAMPs and cytokines, and neutrophil infiltration in CRSwNP. In DNPCs, ATP and IL-1α induced the expression of IL-8 and CXCL-1. Macrophage was found to be the predominant cell type positive for p-MLKL in CRSwNP. Concomitant treatment with TNF-α and IFN-γ, which were abundantly present in CRSwNP, triggered marked necroptosis in THP-1 cells.Necroptosis induced by TNF-α and IFN-γ may facilitate the production and release of a myriad of proinflammatory cytokines and entailed neutrophil infiltration to exacerbate inflammation in CRSwNP.
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI
更新
PDF的下载单位、IP信息已删除 (2025-6-4)

科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
兴奋的乐巧完成签到,获得积分10
刚刚
听说现在你成了大锦鲤完成签到,获得积分10
刚刚
糊涂的冰凡完成签到,获得积分10
1秒前
2秒前
大模型应助HMG1COA采纳,获得10
2秒前
2秒前
4秒前
4秒前
丘山发布了新的文献求助10
4秒前
6秒前
6秒前
ding应助Friday采纳,获得10
7秒前
酷波er应助PatrickWu采纳,获得10
7秒前
好好发布了新的文献求助10
8秒前
Charles关注了科研通微信公众号
8秒前
糊涂塌客完成签到,获得积分10
8秒前
科研助手6应助郭晗采纳,获得10
9秒前
heyihao应助郭晗采纳,获得10
9秒前
大模型应助药毛儿采纳,获得10
10秒前
我不是阿良完成签到,获得积分20
10秒前
1351567822应助无限雨南采纳,获得10
10秒前
liujian发布了新的文献求助10
11秒前
小嘎完成签到 ,获得积分10
12秒前
科研通AI2S应助我不是阿良采纳,获得10
13秒前
CodeCraft应助魔幻诗兰采纳,获得10
14秒前
hongfangpan完成签到 ,获得积分10
14秒前
tramp应助出租耳朵采纳,获得10
14秒前
彩云追月完成签到 ,获得积分10
16秒前
无花果应助风清扬采纳,获得10
17秒前
Fan发布了新的文献求助10
20秒前
平常的紫蓝完成签到,获得积分10
21秒前
22秒前
22秒前
烟花应助111111采纳,获得10
24秒前
河马完成签到,获得积分10
24秒前
科研助手6应助张雯思采纳,获得10
25秒前
25秒前
药毛儿发布了新的文献求助10
27秒前
一洼清泉完成签到,获得积分10
28秒前
hiter完成签到,获得积分10
28秒前
高分求助中
A new approach to the extrapolation of accelerated life test data 1000
ACSM’s Guidelines for Exercise Testing and Prescription, 12th edition 500
‘Unruly’ Children: Historical Fieldnotes and Learning Morality in a Taiwan Village (New Departures in Anthropology) 400
Indomethacinのヒトにおける経皮吸収 400
Phylogenetic study of the order Polydesmida (Myriapoda: Diplopoda) 370
基于可调谐半导体激光吸收光谱技术泄漏气体检测系统的研究 350
Robot-supported joining of reinforcement textiles with one-sided sewing heads 320
热门求助领域 (近24小时)
化学 材料科学 医学 生物 工程类 有机化学 生物化学 物理 内科学 纳米技术 计算机科学 化学工程 复合材料 遗传学 基因 物理化学 催化作用 冶金 细胞生物学 免疫学
热门帖子
关注 科研通微信公众号,转发送积分 3988827
求助须知:如何正确求助?哪些是违规求助? 3531197
关于积分的说明 11252739
捐赠科研通 3269830
什么是DOI,文献DOI怎么找? 1804815
邀请新用户注册赠送积分活动 881915
科研通“疑难数据库(出版商)”最低求助积分说明 809028