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牛乳铁蛋白和嵌合乳铁蛋白可预防和破坏 Caco-2 细胞中的鼠伤寒沙门氏菌生物膜。

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

机构信息

Integral Postgraduate Program in Biotechnology, FCQB, UAS, 80010, Culiacan, Sinaloa, Mexico.

School of Medicine, Autonomous University of Sinaloa, 80019 Culiacan, Sinaloa, Mexico.

出版信息

Biochem Cell Biol. 2024 Dec 1;102(6):515-525. doi: 10.1139/bcb-2024-0100. Epub 2024 Sep 18.

Abstract

Salmonellosis is a common foodborne disease caused by 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 Typhimurium ATCC 14028 or an MDR strain. The inhibitory activity of planktonic bacteria, prevention of biofilm formation, and destruction of biofilms of 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 (75-1000 µM) and LFchimera (1-20 µM) inhibited more than 95% of Typhimurium planktonic growth cultures (ATCC 14028 and MDR). In addition, bLF (600, 800, and 1000 µM) and LFchimera (10 and 20 µM) prevented more than 98% of . Typhimurium adherence and biofilm formation on Caco-2 cells. Finally, bLF (600 and 1000 µM) and LFchimera (10 and 20 µM) destroyed more than 80% of Typhimurium biofilms established on abiotic and Caco-2 cells. In conclusion, bLF and LFchimeras have the potential to inhibit and destroy Typhimurium biofilms.

摘要

肠炎沙门氏菌病是一种常见的食源性疾病,由细菌引起。多重耐药(MDR)鼠伤寒沙门氏菌血清型的出现,以及沙门氏菌形成生物膜的能力,导致其在宿主和非宿主环境中具有耐药性和持久性。需要新的策略来治疗或预防沙门氏菌感染。本工作旨在确定牛乳铁蛋白(bLF)和乳铁蛋白嵌合体(LFchimera)在预防或破坏鼠伤寒沙门氏菌(ATCC 14028 或 MDR 株)在非生物表面或 Caco-2 细胞上形成的生物膜中的作用。通过 CFU/mL 定量测定浮游细菌的抑制活性、生物膜形成的预防以及 bLF 和 LFchimera 对非生物表面和 Caco-2 细胞上的鼠伤寒沙门氏菌(ATCC 14028 或 MDR 株)浮游细菌的破坏,并通过用吉姆萨染色样本进行显微镜观察来可视化。bLF(75-1000 μM)和 LFchimera(1-20 μM)抑制超过 95%的鼠伤寒沙门氏菌浮游培养物(ATCC 14028 和 MDR)的生长。此外,bLF(600、800 和 1000 μM)和 LFchimera(10 和 20 μM)预防超过 98%的鼠伤寒沙门氏菌在 Caco-2 细胞上的黏附和生物膜形成。最后,bLF(600 和 1000 μM)和 LFchimera(10 和 20 μM)破坏了在非生物和 Caco-2 细胞上建立的超过 80%的鼠伤寒沙门氏菌生物膜。总之,bLF 和 LFchimera 具有抑制和破坏鼠伤寒沙门氏菌生物膜的潜力。

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