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肺泡细胞蛋白 10-kDa 减轻气道黏液高分泌和炎症。

Club cell 10-kDa protein attenuates airway mucus hypersecretion and inflammation.

机构信息

Dept of Pediatrics, Virginia Commonwealth University School of Medicine, Richmond, VA, USA.

Division of Physiology, School of Nursing and Rehabilitation Sciences, Showa University, Yokohama, Japan.

出版信息

Eur Respir J. 2014 Oct;44(4):1002-10. doi: 10.1183/09031936.00080913. Epub 2014 May 15.

Abstract

Bacterial lipopolysaccharide (LPS) and interleukin (IL)-13 increase mucus secretion and inflammatory cytokine production in normal human bronchial epithelial (NHBE) cells. We evaluated the effect of club cell 10-kDa protein (CC10), an anti-inflammatory protein produced by epithelial cells, on mucus secretion, cell morphology and inflammatory cytokine production. NHBE cells were cultured at an air-liquid interface with CC10 or vehicle and exposed to LPS on day 14. Mucin MUC5AC, IL-8 and granulocyte-macrophage colony-stimulating factor were measured in cell supernatants. MUC5AC and IL-8 mRNA expression were measured by real-time PCR. Western blotting was used to evaluate nuclear factor (NF)-κB and extracellular signal-regulated kinase (ERK) activation. Cells were evaluated histologically. Additionally, NHBE cells were exposed to IL-13 and CC10 for 14 days, and secretion of the mucins MUC5AC and MUC5B was measured. MUC5AC secretion stimulated either by LPS or by IL-13 was attenuated by CC10 at 20 ng·mL(-1) (p<0.05). CC10 at 20 ng·mL(-1) also attenuated IL-8 secretion (p<0.05). MUC5AC and IL-8 mRNA expression were also decreased by CC10 (p<0.05). CC10 attenuated phosphorylation of NF-κB (p<0.05) and ERK1/2 (p<0.05). CC10 attenuates LPS-induced mucus secretion in airway cells, in part due to inhibition of NF-κB and ERK phosphorylation.

摘要

细菌脂多糖 (LPS) 和白细胞介素 (IL)-13 可增加正常人气道上皮 (NHBE) 细胞的黏液分泌和炎症细胞因子产生。我们评估了上皮细胞产生的抗炎蛋白——克拉细胞 10kDa 蛋白 (CC10) 对黏液分泌、细胞形态和炎症细胞因子产生的影响。NHBE 细胞在气-液界面培养,给予 CC10 或载体,并在第 14 天暴露于 LPS。在细胞上清液中测量粘蛋白 MUC5AC、IL-8 和粒细胞-巨噬细胞集落刺激因子。通过实时 PCR 测量 MUC5AC 和 IL-8 mRNA 表达。Western blot 用于评估核因子 (NF)-κB 和细胞外信号调节激酶 (ERK) 的激活。对细胞进行组织学评估。此外,NHBE 细胞暴露于 IL-13 和 CC10 14 天后,测量粘蛋白 MUC5AC 和 MUC5B 的分泌。LPS 或 IL-13 刺激的 MUC5AC 分泌被 20ng·mL(-1) 的 CC10 减弱 (p<0.05)。20ng·mL(-1) 的 CC10 也减弱了 IL-8 分泌 (p<0.05)。CC10 还降低了 MUC5AC 和 IL-8 mRNA 表达 (p<0.05)。CC10 减弱了 NF-κB (p<0.05) 和 ERK1/2 (p<0.05) 的磷酸化。CC10 减弱 LPS 诱导的气道细胞黏液分泌,部分原因是抑制 NF-κB 和 ERK 磷酸化。

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