Abstract
Background: Chronic rhinosinusitis with nasal polyps (CRSwNP) is classified into two subtypes: eosinophilic (ECRSwNP) and non-eosinophilic (NECRSwNP). Although the inflammatory patterns of ECRSwNP have been elucidated, NECRSwNP is poorly understood.
Aims/objectives: The metalloproteinase ADAM-like decysin 1 (ADAMDEC1) has been reported to play a role in the early stages of the inflammatory response. We investigated the role of ADAMDEC1 in the pathogenesis of CRSwNP.
Material and methods: We compared ADAMDEC1 expression in nasal polyp tissue from CRS patients using immunohistochemistry and RT-qPCR. Macrophages were cultured and ADAMDEC1 expression was determined at baseline and after exposure to lipopolysaccharide (LPS).
Results: ADAMDEC1 was virtually undetectable in tissues from control patients but was highly expressed in the NECRSwNP group compared with the ECRSwNP group. In nasal polyp tissues, ADAMDEC1 was expressed by CD68-positive cells, with a positive correlation between ADAMDEC1-positive and CD68-positive cells, and also between ADAMDEC1 and CD68 mRNA levels. Furthermore, stimulation of monocyte-derived macrophages with LPS induced ADAMDEC1 expression.
Conclusions and significance: This study demonstrates that ADAMDEC1 is involved in the pathogenesis of NECRSwNP, and also bacterial endotoxin signalling in macrophages; however, the underlying mechanism remains to be elucidated.
Chinese abstract
背景:伴鼻息肉慢性鼻窦炎(CRSwNP)分为嗜酸性粒细胞(ECRSwNP)和非嗜酸性粒细胞(NECRSwNP)两种亚型。虽然我们已经很清楚ECRSwNP的炎症型式, 但对NECRSwNP的炎症型式还了解甚少。
目的:金属蛋白酶 似ADAM癸酸1(ADAMDEC1)在炎症反应的早期阶段发挥作用已有报道。我们调查了似ADAM癸酸1在CRSwNP发病机制中的作用。
材料和方法:我们使用免疫组织化学和RT-qPCR比较了慢性鼻窦炎患者的鼻息肉组织中的ADAMDEC1表达。我们培养了巨噬细胞, 并在暴露前和暴露于脂多糖(LPS)后测定ADAMDEC1表达。
结果:ADAMDEC1在对照组患者的组织中几乎检测不到, 但与ECRSwNP组相比, 它在NECRSwNP组中显示高表达。在鼻息肉组织中, ADAMDEC1由CD68阳性细胞表达;ADAMDEC1阳性细胞和CD68阳性细胞之间以及ADAMDEC1和CD68 mRNA水平之间呈正相关。此外, 单核细胞来源的巨噬细胞对LPC的刺激诱导了ADAMDEC1表达。
结论和意义:本研究表明, ADAMDEC1参与NECRSwNP的发病机制, 也参与巨噬细胞内的细菌内毒素信号转导; 然而, 其基本机制仍有待阐明。
Disclosure statement
No potential conflict of interest was reported by the authors.
Acknowledgements
This work was supported by JSPS KAKENHI Grant number JP16K20281. We thank Simon Teteris, PhD, from the Edanz Group (www.edanzediting.com/ac), for editing the English text of a draft of this manuscript..