原標(biāo)題：慢性鼻竇炎鼻息肉源性嗜酸粒細(xì)胞脂肪酸代謝失調(diào)
　　背景：嗜酸粒細(xì)胞是一種多功能粒細(xì)胞，能夠釋放多種細(xì)胞因子、趨化因子和脂質(zhì)介質(zhì)。我們以前報(bào)道過(guò)嚴(yán)重哮喘患者外周血來(lái)源的嗜酸粒細(xì)胞脂肪酸代謝失調(diào)，但是過(guò)敏性炎癥組織中嗜酸粒細(xì)胞的功能特征在很大程度上仍未被檢測(cè)出來(lái)。
　　方法：我們建立了一種從嗜酸性鼻竇炎（NP-EOS）患者鼻息肉中分離CD69hi CCR3low CXCR4- siglec-8int 嗜酸粒細(xì)胞的方法，并與健康受試者外周血來(lái)源的嗜酸粒細(xì)胞（PB-EOS）進(jìn)行脂質(zhì)組學(xué)、蛋白質(zhì)組學(xué)和轉(zhuǎn)錄組學(xué)的多組學(xué)分析，以分析NP-EOS。
　　結(jié)果：脂源性分析顯示前列腺素和15-脂氧合酶（15-lox）衍生介質(zhì)的合成受損，白三烯D4的產(chǎn)生選擇性上調(diào)。此外，蛋白質(zhì)組學(xué)和轉(zhuǎn)錄組學(xué)揭示了導(dǎo)致脂質(zhì)代謝失調(diào)的特異性酶（ggt5、dpep2和15-lox）的表達(dá)變化。獨(dú)創(chuàng)性途徑分析表明2型細(xì)胞因子和模式識(shí)別受體通路的重要性。用嗜酸粒細(xì)胞激活劑IL-5、GM-CSF和TLR2、NOD2受體激動(dòng)劑可以模擬觀察到脂質(zhì)代謝變化。
　　結(jié)論：炎性組織源性嗜酸粒細(xì)胞具有一種特殊的表型，其脂肪酸代謝失調(diào)可作為治療的靶向，以控制嗜酸粒細(xì)胞性炎癥疾病。


延伸閱讀
Allergy：                                                                                                    
[IF:6.048]
Dysregulated fatty acid metabolism in nasal polyp-derived eosinophils from patients with chronic rhinosinusitis  
DOI: 10.1111/all.13726  
Background:
Eosinophils are multifunctional granulocytes capable of releasing various cytokines, chemokines, and lipid mediators. We previously reported dysregulated fatty acid metabolism in peripheral blood-derived eosinophils from patients with severe asthma.However, functional characteristics of eosinophils present in allergic inflammatory tissues remains largely uncharacterized.
Methods: 
We established a method for isolating CD69hi CCR3low CXCR4- siglec-8int eosinophils from nasal polyps of patients with eosinophilic rhinosinusitis (NP-EOS).Multi-omics analysis including lipidomics, proteomics, and transcriptomics was performed to analyze NP-EOS as compared with peripheral blood-derived eosinophils from healthy subjects (PB-EOS). 
Results: Lipidomic analysis revealed impaired synthesis of prostaglandins and 15-lipoxygenase (15-LOX)-derived mediators, and selective upregulation of leukotriene D4 production. Furthermore, proteomics and transcriptomics revealed changes in the expression of specific enzymes (GGT5, DPEP2, and 15-LOX) responsible for dysregulated lipid metabolism. Ingenuity pathway analysis indicated the importance of type 2 cytokines and pattern recognition receptor pathways. Stimulation of PB-EOS with eosinophil activators IL-5, GM-CSF, and agonists of TLR2 and NOD2 mimicked the observed changes in lipid metabolism.
Conclusion: 
Inflammatory tissue-derived eosinophils possess a specific phenotype with dysregulated fatty acid metabolism that may be targeted therapeutically to control eosinophilic inflammatory diseases.
First Author:
Jun Miyata
Corresponding authorLaboratory for Metabolomics RIKEN Center for Integrative Medical Sciences 1-7-22 Suehirocho, Tsurumi-ku, Yokohama, Kanagawa 230-0045, Japan
All Authors:
Jun Miyata, Koichi Fukunaga, Yusuke Kawashima, Takashi Watanabe, Akina Saitoh,Tomomi Hirosaki, Yasutomo Araki, Toru Kikawada, Tomoko Betsuyaku, Osamu Ohara,Makoto Arita
　　創(chuàng)建過(guò)敏性疾病的科研、科普知識(shí)交流平臺(tái)，為過(guò)敏患者提供專(zhuān)業(yè)診斷、治療、預(yù)防的共享平臺(tái)。