Bovine lactoferrin and chimera lactoferrin prevent and destroy Salmonella Typhimurium biofilms in Caco-2 cells.

IF 4.6 Q2 MATERIALS SCIENCE, BIOMATERIALS ACS Applied Bio Materials Pub Date : 2024-09-18 DOI:10.1139/bcb-2024-0100
Laura E Quintero-Martínez,Adrian Canizalez-Roman,Uriel A Angulo-Zamudio,Hector Flores-Villaseñor,Jorge A Velazquez-Roman,Jan G M Bolscher,Kamran Nazmi,Nidia Leon-Sicairos
{"title":"Bovine lactoferrin and chimera lactoferrin prevent and destroy Salmonella Typhimurium biofilms in Caco-2 cells.","authors":"Laura E Quintero-Martínez,Adrian Canizalez-Roman,Uriel A Angulo-Zamudio,Hector Flores-Villaseñor,Jorge A Velazquez-Roman,Jan G M Bolscher,Kamran Nazmi,Nidia Leon-Sicairos","doi":"10.1139/bcb-2024-0100","DOIUrl":null,"url":null,"abstract":"Salmonellosis is a common foodborne disease caused by Salmonella bacteria. The emergence of multidrug-resistant (MDR) Salmonella serotypes, such as Typhimurium, and Salmonella's ability to form biofilms contribute to their resistance and persistence in host and non-host environments. New strategies are needed to treat or prevent Salmonella infections. This work aimed to determine the effect of the bovine lactoferrin (bLF) and lactoferrin chimera (LFchimera) in preventing or disrupting biofilms formed on abiotic surfaces or Caco-2 cells by Salmonella Typhimurium ATCC 14028 or an MDR strain. The inhibitory activity of planktonic bacteria, prevention of biofilm formation, and destruction of biofilms of S. Typhimurium (ATCC 14028 or MDR strain) on the abiotic surface and Caco-2 cells of bLF and LFchimera were quantified by CFU/ml and visualized by microscopy using Giemsa-stained samples. bLF (75-1000µM) and LFchimera (1-20µM) inhibited more than 95% of S. Typhimurium planktonic growth cultures (ATCC 14028 and MDR). In addition, bLF (600, 800, and 1000 µM) and LFchimera (10 and 20µM) prevented more than 98% of S. Typhimurium adherence and biofilm formation on Caco-2 cells. Finally, bLF (600 and 1000 µM) and LFchimera (10 and 20µM) destroyed more than 80% of S. Typhimurium biofilms established on abiotic and Caco-2 cells. In conclusion, bLF and LF chimeras have the potential to inhibit and destroy S. Typhimurium biofilms.","PeriodicalId":2,"journal":{"name":"ACS Applied Bio Materials","volume":null,"pages":null},"PeriodicalIF":4.6000,"publicationDate":"2024-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"ACS Applied Bio Materials","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1139/bcb-2024-0100","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"MATERIALS SCIENCE, BIOMATERIALS","Score":null,"Total":0}
引用次数: 0

Abstract

Salmonellosis is a common foodborne disease caused by Salmonella bacteria. The emergence of multidrug-resistant (MDR) Salmonella serotypes, such as Typhimurium, and Salmonella's ability to form biofilms contribute to their resistance and persistence in host and non-host environments. New strategies are needed to treat or prevent Salmonella infections. This work aimed to determine the effect of the bovine lactoferrin (bLF) and lactoferrin chimera (LFchimera) in preventing or disrupting biofilms formed on abiotic surfaces or Caco-2 cells by Salmonella Typhimurium ATCC 14028 or an MDR strain. The inhibitory activity of planktonic bacteria, prevention of biofilm formation, and destruction of biofilms of S. Typhimurium (ATCC 14028 or MDR strain) on the abiotic surface and Caco-2 cells of bLF and LFchimera were quantified by CFU/ml and visualized by microscopy using Giemsa-stained samples. bLF (75-1000µM) and LFchimera (1-20µM) inhibited more than 95% of S. Typhimurium planktonic growth cultures (ATCC 14028 and MDR). In addition, bLF (600, 800, and 1000 µM) and LFchimera (10 and 20µM) prevented more than 98% of S. Typhimurium adherence and biofilm formation on Caco-2 cells. Finally, bLF (600 and 1000 µM) and LFchimera (10 and 20µM) destroyed more than 80% of S. Typhimurium biofilms established on abiotic and Caco-2 cells. In conclusion, bLF and LF chimeras have the potential to inhibit and destroy S. Typhimurium biofilms.
查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
牛乳铁蛋白和嵌合体乳铁蛋白可防止和破坏 Caco-2 细胞中的鼠伤寒沙门氏菌生物膜。
沙门氏菌病是由沙门氏菌引起的一种常见食源性疾病。耐多药(MDR)沙门氏菌血清型(如伤寒沙门氏菌)的出现,以及沙门氏菌形成生物膜的能力,导致了它们的耐药性以及在宿主和非宿主环境中的持久性。治疗或预防沙门氏菌感染需要新的策略。这项工作旨在确定牛乳铁蛋白(bLF)和乳铁蛋白嵌合体(LFchimera)在预防或破坏伤寒沙门氏菌 ATCC 14028 或 MDR 菌株在非生物表面或 Caco-2 细胞上形成的生物膜方面的效果。bLF 和 LFchimera 对非生物表面和 Caco-2 细胞上 Typhimurium 沙门氏菌(ATCC 14028 或 MDR 菌株)浮游菌的抑制活性、生物膜形成的阻止作用和生物膜的破坏作用均以 CFU/ml 进行量化,并使用 Giemsa 染色样本进行显微镜观察。bLF(75-1000µM)和 LFchimera(1-20µM)对 95% 以上的伤寒杆菌浮游生长培养物(ATCC 14028 和 MDR)具有抑制作用。此外,bLF(600、800 和 1000 µM)和 LFchimera(10 和 20 µM)对 Caco-2 细胞上的伤寒杆菌粘附和生物膜形成的抑制率超过 98%。最后,bLF(600 微摩尔和 1000 微摩尔)和 LFchimera(10 微摩尔和 20 微摩尔)破坏了 80% 以上在非生物细胞和 Caco-2 细胞上形成的伤寒杆菌生物膜。总之,bLF 和 LF 嵌合体具有抑制和破坏伤寒杆菌生物膜的潜力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
ACS Applied Bio Materials
ACS Applied Bio Materials Chemistry-Chemistry (all)
CiteScore
9.40
自引率
2.10%
发文量
464
期刊最新文献
A Systematic Review of Sleep Disturbance in Idiopathic Intracranial Hypertension. Advancing Patient Education in Idiopathic Intracranial Hypertension: The Promise of Large Language Models. Anti-Myelin-Associated Glycoprotein Neuropathy: Recent Developments. Approach to Managing the Initial Presentation of Multiple Sclerosis: A Worldwide Practice Survey. Association Between LACE+ Index Risk Category and 90-Day Mortality After Stroke.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1