The preventive effects of Lactobacillus casei 03 on Escherichia coli-induced mastitis in vitro and in vivo.

IF 4.4 3区 医学 Q2 IMMUNOLOGY
Ke Li, Ming Yang, Mengyue Tian, Li Jia, Yinghao Wu, Jinliang Du, Lining Yuan, Lianmin Li, Yuzhong Ma
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引用次数: 0

Abstract

Background: Lactobacillus casei possesses many kinds of bioactivities, such as anti-inflammation and anti-oxidant, and has been applied to treating multiple inflammatory diseases. However, its role in mastitis prevention has remained ambiguous.

Methods: This study aimed to examine the mechanisms underlying the preventive effects of L. casei 03 against E. coli- mastitis utilizing bovine mammary epithelial cells (BMECs) and a mouse model.

Results: In vitro assays revealed pretreatment with L. casei 03 reduced the apoptotic ratio and the mRNA expression levels of IL1β, IL6 and TNFα and suppressed phosphorylation of p65, IκBα, p38, JNK and ERK in the NF-κB signaling pathway and MAPK signaling pathway. Furthermore, in vivo tests indicated that intramammary infusion of L. casei 03 relieved pathological changes, reduced the secretion of IL1β, IL6 and TNFα and MPO activity in the mouse mastitis model.

Conclusions: These data suggest that L. casei 03 exerts protective effects against E. coli-induced mastitis in vitro and in vivo and may hold promise as a novel agent for the prevention and treatment of mastitis.

干酪乳杆菌 03 在体外和体内对大肠杆菌诱发的乳腺炎的预防作用。
背景:干酪乳杆菌具有抗炎、抗氧化等多种生物活性,已被用于治疗多种炎症性疾病。然而,它在乳腺炎预防中的作用仍不明确:本研究旨在利用牛乳腺上皮细胞(BMECs)和小鼠模型研究干酪乳杆菌 03 预防大肠杆菌性乳腺炎的作用机制:结果:体外试验显示,使用干酪乳杆菌 03 的预处理可降低细胞凋亡率以及 IL1β、IL6 和 TNFα 的 mRNA 表达水平,并抑制 NF-κB 信号通路和 MAPK 信号通路中 p65、IκBα、p38、JNK 和 ERK 的磷酸化。此外,体内试验表明,在小鼠乳腺炎模型中,乳房内灌注干酪乳杆菌 03 可缓解病理变化,减少 IL1β、IL6 和 TNFα 的分泌以及 MPO 活性:这些数据表明,干酪乳杆菌 03 在体外和体内对大肠杆菌诱发的乳腺炎具有保护作用,有望成为预防和治疗乳腺炎的新型药物。
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来源期刊
CiteScore
7.90
自引率
0.00%
发文量
18
审稿时长
>12 weeks
期刊介绍: Journal of Inflammation welcomes research submissions on all aspects of inflammation. The five classical symptoms of inflammation, namely redness (rubor), swelling (tumour), heat (calor), pain (dolor) and loss of function (functio laesa), are only part of the story. The term inflammation is taken to include the full range of underlying cellular and molecular mechanisms involved, not only in the production of the inflammatory responses but, more importantly in clinical terms, in the healing process as well. Thus the journal covers molecular, cellular, animal and clinical studies, and related aspects of pharmacology, such as anti-inflammatory drug development, trials and therapeutic developments. It also considers publication of negative findings. Journal of Inflammation aims to become the leading online journal on inflammation and, as online journals replace printed ones over the next decade, the main open access inflammation journal. Open access guarantees a larger audience, and thus impact, than any restricted access equivalent, and increasingly so, as the escalating costs of printed journals puts them outside University budgets. The unrestricted access to research findings in inflammation aids in promoting dynamic and productive dialogue between industrial and academic members of the inflammation research community, which plays such an important part in the development of future generations of anti-inflammatory therapies.
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