LPS induces pro-inflammatory response in mastitis mice and mammary epithelial cells: Possible involvement of NF-κB signaling and OPN

H.-B. Xiao , C.-R. Wang , Z.-K. Liu , J.-Y. Wang
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引用次数: 24

Abstract

Background

Lipopolysaccharide (LPS) has pro-inflammatory properties. This study was conducted to determine whether the LPS induced pro-inflammatory response in a model of mastitis and in mouse mammary epithelial cells (MEC).

Methods

To investigate the effects of LPS in vivo, 50 μL of a solution of LPS (20 ng/μL) were infused into the mammary glands of mice. To study the effects of LPS in vitro, MEC were exposed to LPS (20 μg/mL) for 24 h. Activation of nuclear factor kB (NF-κB) and myeloperoxidase (MPO) were studied. Production of pro-inflammatory cytokines (interleukin-6 [IL-6], tumor necrosis factor-alpha [TNF-alpha], interleukin-1 beta [IL-1beta]) and expression of osteopontin (OPN) were also evaluated.

Results

After LPS administration, route of NF-κB signaling is activated and the activity of MPO is increased. Furthermore, LPS increases the expression of OPN and production of TNF-alpha, IL-6 and IL-1beta.

Conclusions

Present results demonstrate that LPS induces a pro-inflammatory response in a murine model of mastitis and suggest the involvement of the NF-κB pathway and OPN.

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LPS诱导乳腺炎小鼠和乳腺上皮细胞的促炎反应:可能与NF-κB信号和OPN有关
背景:脂多糖(LPS)具有促炎特性。本研究旨在确定LPS是否在乳腺炎模型和小鼠乳腺上皮细胞(MEC)中诱导促炎反应。方法将LPS溶液(20 ng/μL)灌胃50 μL,观察LPS对小鼠乳腺的影响。为了研究LPS对MEC的体外作用,我们将MEC暴露于LPS (20 μg/mL)中24 h,观察其对核因子kB (NF-κB)和髓过氧化物酶(MPO)的激活作用。还评估了促炎细胞因子(白细胞介素-6 [IL-6]、肿瘤坏死因子- α [tnf - α]、白细胞介素-1 β [il -1 β])的产生和骨桥蛋白(OPN)的表达。结果LPS处理后,NF-κB信号通路被激活,MPO活性升高。此外,LPS增加了OPN的表达和tnf - α、IL-6和il -1 β的产生。结论LPS在小鼠乳腺炎模型中诱导了促炎反应,提示其参与了NF-κB通路和OPN通路。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Pathologie-biologie
Pathologie-biologie 医学-病理学
自引率
0.00%
发文量
0
审稿时长
6-12 weeks
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