• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

短期与长期培养 A549 细胞评估脂多糖对氧化应激、表面活性蛋白和抗菌肽 LL-37 的影响

Short-Term versus Long-Term Culture of A549 Cells for Evaluating the Effects of Lipopolysaccharide on Oxidative Stress, Surfactant Proteins and Cathelicidin LL-37.

机构信息

Department of Physiology and Biomedical Center Martin, Jessenius Faculty of Medicine in Martin, Comenius University in Bratislava, 03601 Martin, Slovakia.

Division of Molecular Medicine, Biomedical Center Martin, Jessenius Faculty of Medicine in Martin, Comenius University in Bratislava, 03601 Martin, Slovakia.

出版信息

Int J Mol Sci. 2020 Feb 9;21(3):1148. doi: 10.3390/ijms21031148.

DOI:10.3390/ijms21031148
PMID:32050475
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7036965/
Abstract

Alveolar epithelial type II (ATII) cells and their proper function are essential for maintaining lung integrity and homeostasis. However, they can be damaged by lipopolysaccharide (LPS) during Gram-negative bacterial infection. Thus, this study evaluated and compared the effects of LPS on short and long-term cultures of A549 cells by determining the cell viability, levels of oxidative stress and antimicrobial peptide cathelicidin LL-37 and changes in the expression of surfactant proteins (SPs). Moreover, we compared A549 cell response to LPS in the presence of different serum concentrations. Additionally, the effect of -acetylcysteine (NAC) on LPS-induced oxidative stress as a possible treatment was determined. Our results indicate that A549 cells are relatively resistant to LPS and able to maintain integrity even at high LPS concentrations. Their response to endotoxin is partially dependent on serum concentration. NAC failed to lower LPS-induced oxidative stress in A549 cells. Finally, LPS modulates SP gene expression in A549 cells in a time dependent manner and differences between short and long-term cultures were present. Our results support the idea that long-term cultivation of A549 cells could promote a more ATII-like phenotype and thus could be a more suitable model for ATII cells, especially for in vitro studies dealing with surfactant production.

摘要

肺泡上皮细胞 II 型 (ATII) 及其正常功能对于维持肺的完整性和内稳态至关重要。然而,在革兰氏阴性菌感染过程中,脂多糖 (LPS) 会损伤这些细胞。因此,本研究通过测定细胞活力、氧化应激水平和抗菌肽 cathelicidin LL-37 水平以及表面活性剂蛋白 (SP) 的表达变化,评估并比较了 LPS 对 A549 细胞短期和长期培养的影响。此外,我们比较了 A549 细胞在不同血清浓度下对 LPS 的反应。还确定了 -乙酰半胱氨酸 (NAC) 作为可能的治疗方法对 LPS 诱导的氧化应激的影响。结果表明,A549 细胞对 LPS 具有相对抗性,即使在高 LPS 浓度下也能保持完整性。它们对内毒素的反应部分取决于血清浓度。NAC 未能降低 A549 细胞中 LPS 诱导的氧化应激。最后,LPS 以时间依赖的方式调节 A549 细胞中 SP 基因的表达,并且在短期和长期培养之间存在差异。我们的结果支持这样一种观点,即 A549 细胞的长期培养可能会促进更类似于 ATII 细胞的表型,因此对于涉及表面活性剂产生的体外研究,特别是对于体外研究,可能是更合适的 ATII 细胞模型。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1514/7036965/33d3e3fffb37/ijms-21-01148-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1514/7036965/63cefaac3bcf/ijms-21-01148-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1514/7036965/b762c2efcb9c/ijms-21-01148-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1514/7036965/3aab6f5d7f30/ijms-21-01148-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1514/7036965/4552fceacf6a/ijms-21-01148-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1514/7036965/7747fa1b740d/ijms-21-01148-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1514/7036965/2d1dab33c73c/ijms-21-01148-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1514/7036965/2afe12b76883/ijms-21-01148-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1514/7036965/33d3e3fffb37/ijms-21-01148-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1514/7036965/63cefaac3bcf/ijms-21-01148-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1514/7036965/b762c2efcb9c/ijms-21-01148-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1514/7036965/3aab6f5d7f30/ijms-21-01148-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1514/7036965/4552fceacf6a/ijms-21-01148-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1514/7036965/7747fa1b740d/ijms-21-01148-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1514/7036965/2d1dab33c73c/ijms-21-01148-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1514/7036965/2afe12b76883/ijms-21-01148-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1514/7036965/33d3e3fffb37/ijms-21-01148-g008.jpg

相似文献

1
Short-Term versus Long-Term Culture of A549 Cells for Evaluating the Effects of Lipopolysaccharide on Oxidative Stress, Surfactant Proteins and Cathelicidin LL-37.短期与长期培养 A549 细胞评估脂多糖对氧化应激、表面活性蛋白和抗菌肽 LL-37 的影响
Int J Mol Sci. 2020 Feb 9;21(3):1148. doi: 10.3390/ijms21031148.
2
Toll-like receptor 2-mediated sequential activation of MyD88 and MAPKs contributes to lipopolysaccharide-induced sp-a gene expression in human alveolar epithelial cells.Toll 样受体 2 介导的 MyD88 和 MAPKs 的顺序激活有助于脂多糖诱导的人肺泡上皮细胞 sp-a 基因表达。
Immunobiology. 2011 Jun;216(6):707-14. doi: 10.1016/j.imbio.2010.10.009. Epub 2010 Nov 4.
3
Lipopolysaccharide induces apoptotic insults to human alveolar epithelial A549 cells through reactive oxygen species-mediated activation of an intrinsic mitochondrion-dependent pathway.脂多糖通过活性氧介导的内在线粒体依赖性途径的激活诱导人肺泡上皮 A549 细胞发生凋亡损伤。
Arch Toxicol. 2011 Mar;85(3):209-18. doi: 10.1007/s00204-010-0585-x. Epub 2010 Sep 17.
4
Effects of Ghrelin on iNOS-Derived NO Promoted LPS-Induced Pulmonary Alveolar Epithelial A549 Cells Apoptosis.胃饥饿素对诱导型一氧化氮合酶衍生的一氧化氮促进脂多糖诱导的肺泡上皮A549细胞凋亡的影响。
Cell Physiol Biochem. 2018;49(5):1840-1855. doi: 10.1159/000493630. Epub 2018 Sep 19.
5
The collectin SP-A and its trimeric recombinant fragment protect alveolar epithelial cells from the cytotoxic and proinflammatory effects of human cathelicidin .胶原凝集素 SP-A 及其三聚体重组片段可保护肺泡上皮细胞免受人源抗菌肽的细胞毒性和促炎作用的影响。
Front Immunol. 2022 Aug 29;13:994328. doi: 10.3389/fimmu.2022.994328. eCollection 2022.
6
Melatonin prevents LPS-induced epithelial-mesenchymal transition in human alveolar epithelial cells via the GSK-3β/Nrf2 pathway.褪黑素通过 GSK-3β/Nrf2 通路预防脂多糖诱导的人肺泡上皮细胞上皮-间充质转化。
Biomed Pharmacother. 2020 Dec;132:110827. doi: 10.1016/j.biopha.2020.110827. Epub 2020 Oct 13.
7
Augmentation of the lipopolysaccharide-neutralizing activities of human cathelicidin CAP18/LL-37-derived antimicrobial peptides by replacement with hydrophobic and cationic amino acid residues.通过用疏水和阳离子氨基酸残基取代来增强人cathelicidin CAP18/LL-37衍生抗菌肽的脂多糖中和活性。
Clin Diagn Lab Immunol. 2002 Sep;9(5):972-82. doi: 10.1128/cdli.9.5.972-982.2002.
8
Molecular mechanisms of lipopolysaccharide-caused induction of surfactant protein-A gene expression in human alveolar epithelial A549 cells.脂多糖诱导人肺泡上皮A549细胞表面活性蛋白-A基因表达的分子机制
Toxicol Lett. 2009 Dec 15;191(2-3):132-9. doi: 10.1016/j.toxlet.2009.08.015. Epub 2009 Aug 25.
9
Cathelicidin-mediated lipopolysaccharide signaling via intracellular TLR4 in colonic epithelial cells evokes CXCL8 production.抗菌肽介导的细胞内 TLR4 信号通路在结肠上皮细胞中引发 CXCL8 的产生。
Gut Microbes. 2020 Nov 9;12(1):1785802. doi: 10.1080/19490976.2020.1785802. Epub 2020 Jul 13.
10
Antimicrobial and chemoattractant activity, lipopolysaccharide neutralization, cytotoxicity, and inhibition by serum of analogs of human cathelicidin LL-37.人源杀菌肽LL-37类似物的抗菌和趋化活性、脂多糖中和作用、细胞毒性及血清抑制作用
Antimicrob Agents Chemother. 2005 Jul;49(7):2845-50. doi: 10.1128/AAC.49.7.2845-2850.2005.

引用本文的文献

1
Prolonged in vitro anti-bacterial, anti-inflammatory, and surfactant-promoting effects of volatile anesthetics.挥发性麻醉剂的体外抗菌、抗炎和促进表面活性剂作用的延长效应。
BMC Pulm Med. 2025 Sep 9;25(1):425. doi: 10.1186/s12890-025-03849-w.
2
CFTR Modulators Counteract F508del CFTR Functional Defects in a Pancreatic Epithelial Model of Cystic Fibrosis.CFTR调节剂可抵消囊性纤维化胰腺上皮模型中F508del CFTR的功能缺陷。
Life (Basel). 2025 Aug 19;15(8):1315. doi: 10.3390/life15081315.
3
Exploiting gasdermin-mediated pyroptosis for enhanced antimicrobial activity of phage endolysin against .

本文引用的文献

1
A Peptide Inhibitor of NADPH Oxidase (NOX2) Activation Markedly Decreases Mouse Lung Injury and Mortality Following Administration of Lipopolysaccharide (LPS).一种 NADPH 氧化酶(NOX2)激活的肽抑制剂显著降低了给予脂多糖(LPS)后小鼠的肺损伤和死亡率。
Int J Mol Sci. 2019 May 15;20(10):2395. doi: 10.3390/ijms20102395.
2
Alveolar-Capillary Membrane-Related Pulmonary Cells as a Target in Endotoxin-Induced Acute Lung Injury.肺泡-毛细血管膜相关肺细胞作为内毒素诱导的急性肺损伤的靶点。
Int J Mol Sci. 2019 Feb 15;20(4):831. doi: 10.3390/ijms20040831.
3
polysaccharides inhibit cellular apoptosis and autophagy induced by lipopolysaccharide in A549 cells through sirtuin 1 activation.
利用gasdermin介导的细胞焦亡增强噬菌体溶菌酶的抗菌活性 针对…… (原文此处不完整)
mSystems. 2025 Jan 21;10(1):e0110624. doi: 10.1128/msystems.01106-24. Epub 2024 Dec 23.
4
Oxidative stress: fundamentals and advances in quantification techniques.氧化应激:量化技术的基础与进展
Front Chem. 2024 Oct 7;12:1470458. doi: 10.3389/fchem.2024.1470458. eCollection 2024.
5
Role of Lipopolysaccharides in the Inflammation and Pyroptosis of Alveolar Epithelial Cells in Acute Lung Injury and Acute Respiratory Distress Syndrome.脂多糖在急性肺损伤和急性呼吸窘迫综合征中肺泡上皮细胞炎症和焦亡中的作用
J Inflamm Res. 2024 Aug 30;17:5855-5869. doi: 10.2147/JIR.S479051. eCollection 2024.
6
Correlating transcription and protein expression profiles of immune biomarkers following lipopolysaccharide exposure in lung epithelial cells.脂多糖暴露后肺上皮细胞中免疫生物标志物的转录与蛋白质表达谱的相关性研究
PLoS One. 2024 Apr 23;19(4):e0293680. doi: 10.1371/journal.pone.0293680. eCollection 2024.
7
Effect of Atomized Black Maca ( Supplementation in the Cryopreservation of Alpaca ( Epididymal Spermatozoa.雾化黑玛卡对羊驼附睾精子冷冻保存的影响。
Animals (Basel). 2023 Jun 21;13(13):2054. doi: 10.3390/ani13132054.
8
Antioxidant Biomaterials in Cutaneous Wound Healing and Tissue Regeneration: A Critical Review.皮肤伤口愈合和组织再生中的抗氧化生物材料:综述
Antioxidants (Basel). 2023 Mar 23;12(4):787. doi: 10.3390/antiox12040787.
9
Investigating the cytotoxic redox mechanism of PFOS within Hep G2 by hyperspectral-assisted scanning electrochemical microscopy.应用高光谱辅助扫描电化学显微镜研究全氟辛烷磺酸(PFOS)在 Hep G2 细胞中的细胞毒性氧化还原机制。
Analyst. 2022 Sep 26;147(19):4356-4364. doi: 10.1039/d2an00904h.
10
Fetal Lung-Derived Exosomes in Term Labor Amniotic Fluid Induce Amniotic Membrane Senescence.足月分娩羊水来源的胎儿肺外泌体诱导羊膜衰老。
Front Cell Dev Biol. 2022 Jul 4;10:889861. doi: 10.3389/fcell.2022.889861. eCollection 2022.
多糖通过激活沉默调节蛋白1抑制脂多糖诱导的A549细胞凋亡和自噬。
Oncol Lett. 2018 Jun;15(6):9609-9616. doi: 10.3892/ol.2018.8554. Epub 2018 Apr 23.
4
Site-specific and endothelial-mediated dysfunction of the alveolar-capillary barrier in response to lipopolysaccharides.脂多糖引起的肺泡毛细血管屏障的部位特异性和内皮介导功能障碍。
J Cell Mol Med. 2018 Feb;22(2):982-998. doi: 10.1111/jcmm.13421. Epub 2017 Dec 5.
5
Downregulation of p300 alleviates LPS-induced inflammatory injuries through regulation of RhoA/ROCK/NF-κB pathways in A549 cells.p300 的下调通过调节 RhoA/ROCK/NF-κB 通路减轻 LPS 诱导的 A549 细胞炎症损伤。
Biomed Pharmacother. 2018 Jan;97:369-374. doi: 10.1016/j.biopha.2017.10.104. Epub 2017 Nov 6.
6
ROS Signaling in the Pathogenesis of Acute Lung Injury (ALI) and Acute Respiratory Distress Syndrome (ARDS).活性氧信号传导在急性肺损伤(ALI)和急性呼吸窘迫综合征(ARDS)发病机制中的作用
Adv Exp Med Biol. 2017;967:105-137. doi: 10.1007/978-3-319-63245-2_8.
7
Pulmonary surfactant and bacterial lipopolysaccharide: the interaction and its functional consequences.肺表面活性物质与细菌脂多糖:相互作用及其功能后果
Physiol Res. 2017 Sep 22;66(Suppl 2):S147-S157. doi: 10.33549/physiolres.933672.
8
When Is an Alveolar Type 2 Cell an Alveolar Type 2 Cell? A Conundrum for Lung Stem Cell Biology and Regenerative Medicine.何时肺泡Ⅱ型细胞才是真正的肺泡Ⅱ型细胞?这是肺干细胞生物学和再生医学面临的一个难题。
Am J Respir Cell Mol Biol. 2017 Jul;57(1):18-27. doi: 10.1165/rcmb.2016-0426PS.
9
Low concentration of oleic acid exacerbates LPS-induced cell death and inflammation in human alveolar epithelial cells.低浓度油酸会加剧脂多糖诱导的人肺泡上皮细胞死亡和炎症。
Exp Lung Res. 2017 Feb;43(1):1-7. doi: 10.1080/01902148.2016.1267823. Epub 2017 Jan 12.
10
Apoptosis and surfactant protein-C expression inhibition induced by lipopolysaccharide in AEC II cell may associate with NF-κB pathway.脂多糖诱导的II型肺泡上皮细胞凋亡及表面活性蛋白-C表达抑制可能与核因子κB通路有关。
J Toxicol Sci. 2017;42(1):53-61. doi: 10.2131/jts.42.53.