Damage-associated molecular patterns stimulate interleukin-33 expression in nasal polyp epithelial cells.
Damage-associated molecular patterns stimulate interleukin-33 expression in nasal polyp epithelial cells.
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DOI：
10.1002/alr.21237
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发表时间：
2014-01
影响因子：
6.4
通讯作者：
Lane, Andrew P.
中科院分区：
文献类型：
--
作者：
Paris, Gina;Pozharskaya, Tatyana;Asempa, Tomefa;Lane, Andrew P.
慢性鼻窦炎伴鼻息肉（CRSwNP）是一种以嗜酸性粒细胞炎症和局部Th 2细胞因子产生为特征的疾病。先天性淋巴样细胞，阐述了Th 2细胞因子最近的特点是在鼻息肉。这些细胞可以被上皮细胞衍生的细胞因子IL-33激活。本研究的目的是确定两种与组织损伤相关的分子（HMGB-1和ATP）是否会引起来源于难治性CRSwNP患者的鼻窦上皮细胞（SNEC）中IL-33的表达。在ESS过程中，从8名受试者和9名对照受试者中获得筛窦组织。组织制备用于免疫组织化学和SNEC气液界面培养。在体外暴露于HMGB 1或ATP后，SNEC被处理用于mRNA提取和免疫细胞化学。通过实时PCR和用抗IL-33抗体的免疫化学染色测定IL-33水平。核内IL-33通常在基底上皮细胞中表达，但在CRSwNP中存在于更多的顶端细胞和核外。SNEC暴露于HMGB-1或ATP导致来源于难治性CRSwNP患者的SNEC中IL-33 mRNA表达的统计学显著增加。这种增加通过IL-33的免疫化学染色在蛋白质水平上反映。组织损伤是治疗无效的息肉中上皮IL-33产生的非特异性触发因素，这可能是CRSwNP中持续嗜酸性炎症的原因。这种共同的途径可能有助于解释为什么多种环境和感染因子与CRSwNP恶化有关。
Chronic rhinosinusitis with nasal polyps (CRSwNP) is a disorder characterized by eosinophilic inflammation and local Th2 cytokine production. Innate lymphoid cells that elaborate Th2 cytokines have recently been characterized within nasal polyps. These cells can be activated by the epithelial cell-derived cytokine IL-33. The objective of this study is to determine whether two molecules associated with tissue damage (HMGB-1 and ATP) elicit expression of IL-33 in sinonasal epithelial cells (SNEC) derived from recalcitrant CRSwNP patients. Ethmoid tissue was obtained from 8 recalcitrant CRSwNP and 9 control subjects during ESS. Tissue was prepared for immunohistochemistry and for SNEC air-liquid interface culture. After exposure to either HMGB1 or ATP in vitro, SNEC were processed for mRNA extraction and immunocytochemistry. IL33 levels were determined by real-time PCR and by immunochemical staining with anti-IL-33 antibody. Intranuclear IL-33 is normally expressed in basal epithelial cells, but is present in more apical cells and outside the nucleus in CRSwNP. Exposure of SNEC to HMGB-1 or ATP resulted in a statistically significant increase in IL-33 mRNA expression in SNEC derived from recalcitrant CRSwNP patients. This increase was reflected at the protein level by immunochemical staining of IL-33. Tissue damage is a non-specific trigger of epithelial IL-33 production in treatment-recalcitrant polyps, which may be responsible for perpetuating eosinophilic inflammation in CRSwNP. This common pathway may help explain why multiple environmental and infectious agents have been implicated in association with CRSwNP exacerbation.
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DOI：
10.1073/pnas.0812690106
发表时间：
2009-06-02
影响因子：
11.1
作者：
Cayrol, Corinne;Girard, Jean-Philippe
通讯作者：
Girard, Jean-Philippe
DOI：
10.1016/j.otohns.2004.09.067
发表时间：
2004-12
期刊：
Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery
影响因子：
--
作者：
Meltzer EO;Hamilos DL;Hadley JA;Lanza DC;Marple BF;Nicklas RA;Bachert C;Baraniuk J;Baroody FM;Benninger MS;Brook I;Chowdhury BA;Druce HM;Durham S;Ferguson B;Gwaltney JM Jr;Kaliner M;Kennedy DW;Lund V;Naclerio R;Pawankar R;Piccirillo JF;Rohane P;Simon R;Slavin RG;Togias A;Wald ER;Zinreich SJ;American Academy of Allergy, Asthma and Immunology;American Academy of Otolaryngic Allergy;American Academy of Otolaryngology-Head and Neck Surgery;American College of Allergy, Asthma and Immunology;American Rhinologic Society
通讯作者：
American Rhinologic Society
DOI：
10.4049/jimmunol.1003020
发表时间：
2011-04-01
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Kouzaki H;Iijima K;Kobayashi T;O'Grady SM;Kita H
通讯作者：
Kita H
影响因子：
4.4
作者：
Kurowska-Stolarska, Mariola;Stolarski, Bartosz;Liew, Foo Y.
通讯作者：
Liew, Foo Y.
影响因子：
7.2
作者：
Fokkens, Wytske J.;Lund, Valerie J.;Zwetsloot, Casper P.
通讯作者：
Zwetsloot, Casper P.