Pro-Resolution Mediator Lipoxin A4 and its Receptor in Upper Airway Inflammation
Pro-Resolution Mediator Lipoxin A4 and its Receptor in Upper Airway Inflammation
复制标题
DOI：
10.1177/000348941312201104
复制
发表时间：
2013-11
期刊：
影响因子：
--
通讯作者：
S. Shimizu;T. Ogawa;S. Seno;H. Kouzaki;Takeshi Shimizu
中科院分区：
文献类型：
--
作者：
S. Shimizu;T. Ogawa;S. Seno;H. Kouzaki;Takeshi Shimizu
目的：炎症的消退是一个由多种抗炎和促消退介质控制的主动过程。脂氧素 A4 是一种内源性脂质介质，是一种潜在的促消退介质，可以减轻炎症。本研究旨在阐明脂氧素 A4 在上呼吸道炎症中的作用。方法：收集慢性鼻窦炎合并鼻息肉病患者、过敏性鼻炎患者和对照受试者的鼻分泌物。通过酶联免疫吸附测定法测定脂氧素A4的浓度。鼻组织是在鼻内手术期间从鼻息肉和下鼻甲获得的。通过逆转录聚合酶链反应检测鼻组织中脂氧合酶（LOX）、脂氧素受体（甲酰肽受体样1；FPRL-1）和半胱氨酰白三烯1型受体（CysLT1R）的mRNA表达。通过免疫组织化学染色确定 FPRL-1 的组织定位。还检查了脂氧素 A4 对气道上皮细胞的体外影响。结果：鼻分泌物中脂氧素A4浓度明显升高，且过敏性鼻炎患者浓度升高。鼻息肉中 5-LOX、15-LOX-1、FPRL-1 和 CysLT1R 的 mRNA 表达量显着高于下鼻甲。 FPRL-1 定位于鼻上皮细胞。脂氧素 A4 通过其受体 FPRL-1 抑制肿瘤坏死因子 α 诱导的气道上皮细胞释放白细胞介素 8。结论：这些结果表明脂氧素 A4 可能在解决上呼吸道炎症中发挥作用。低浓度的脂氧素 A4 可能与上呼吸道的慢性炎症有关。
Objectives: The resolution of inflammation is an active process controlled by several anti-inflammatory and pro-resolution mediators. Lipoxin A4, an endogenous lipid mediator, is a potential pro-resolution mediator that could attenuate inflammation. This study was conducted to elucidate the role of lipoxin A4 in upper airway inflammation. Methods: Nasal secretions were collected from patients with chronic rhinosinusitis with nasal polyposis, patients with allergic rhinitis, and control subjects. The concentration of lipoxin A4 was measured by enzyme-linked immunosorbent assay. Nasal tissues were obtained from nasal polyps and inferior turbinates during endonasal surgery. The mRNA expressions of lipoxygenases (LOXs), lipoxin receptor (formyl peptide receptor-like 1; FPRL-1), and cysteinyl leukotriene type 1 receptor (CysLT1R) in nasal tissues were examined by reverse-transcription polymerase chain reaction. Tissue localization of FPRL-1 was determined by immunohistochemical staining. The in vitro effect of lipoxin A4 on airway epithelial cells was also examined. Results: A significant concentration of lipoxin A4 was found in nasal secretions, and the concentration was increased in patients with allergic rhinitis. The mRNA expressions of 5-LOX, 15-LOX-1, FPRL-1, and CysLT1R were significantly greater in nasal polyps than in inferior turbinates. FPRL-1 was localized in nasal epithelial cells. Lipoxin A4 inhibited tumor necrosis factor α-induced interleukin 8 release from airway epithelial cells via its receptor FPRL-1. Conclusions: These results indicate that lipoxin A4 may play a role in the resolution of upper airway inflammation. A low concentration of lipoxin A4 may be involved in chronic inflammation of the upper airways.