探索鼠李糖乳杆菌 PMC203 在诱导自噬以减轻结核分枝杆菌负担方面的潜力。

IF 5.5 3区 医学 Q1 IMMUNOLOGY
Md Abdur Rahim, Hoonhee Seo, Sukyung Kim, Indrajeet Barman, Fatemeh Ghorbanian, Mohammed Solayman Hossain, Md Sarower Hossen Shuvo, Saebim Lee, Ho-Yeon Song
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引用次数: 0

摘要

结核分枝杆菌是人类历史上一种致命的病原体,每年导致数百万人死亡,因此需要开发新的药物概念。有鉴于此,早先的研究探索了益生菌株鼠李糖乳杆菌(Lactocaseibacillus rhamnosus PMC203)的抗结核潜力,并由此开始关注其作用的分子机制,尤其是自噬作用。在本研究中,基于免疫印迹的检测显示,与未处理组相比,PMC203 处理组的自噬标志物 LC3-II 表达显著。与对照组相比,处理组细胞中的 p62 也明显降低。此外,基于免疫荧光的检测显示,alexa-647-LC3 和 alexa-488-LC3 的荧光强度发生了显著的折叠变化,而 p62 则明显降低。此外,就 LAMP1 和酸性囊泡细胞器而言,溶酶体生物生成明显增加。因此,与未处理组相比,PMC203 诱导的自噬在减少巨噬细胞内结核杆菌负荷方面发挥了重要作用。集落形成单位检测也显示,随着时间的推移,处理组细胞中的结核杆菌数量显著减少。此外,候选菌株还能显著上调自噬诱导基因和溶酶体生物发生基因的表达。总之,这些结果可以丰富我们目前对益生菌介导的结核病自噬的认识,并表明其对创新性管理结核病的意义。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Exploring the potential of Lactocaseibacillus rhamnosus PMC203 in inducing autophagy to reduce the burden of Mycobacterium tuberculosis.

Exploring the potential of Lactocaseibacillus rhamnosus PMC203 in inducing autophagy to reduce the burden of Mycobacterium tuberculosis.

Mycobacterium tuberculosis, a lethal pathogen in human history, causes millions of deaths annually, which demands the development of new concepts of drugs. Considering this fact, earlier research has explored the anti-tuberculosis potential of a probiotic strain, Lactocaseibacillus rhamnosus PMC203, leading to a subsequent focus on the molecular mechanism involved in its effect, particularly on autophagy. In this current study, immunoblotting-based assay exhibited a remarkable expression of autophagy marker LC3-II in the PMC203 treated group compared to an untreated group. A remarkable degradation of p62 was also noticed within treated cells compared to control. Furthermore, the immunofluorescence-based assay showed significant fold change in fluorescence intensity for alexa-647-LC3 and alexa-488-LC3, whereas p62 was degraded noticeably. Moreover, lysosomal biogenesis generation was elevated significantly in terms of LAMP1 and acidic vesicular organelles. As a result, PMC203-induced autophagy played a vital role in reducing M. tuberculosis burden within the macrophages in treated groups compared to untreated group. A colony -forming unit assay also revealed a significant reduction in M. tuberculosis in the treated cells over time. Additionally, the candidate strain significantly upregulated the expression of autophagy induction and lysosomal biogenesis genes. Together, these results could enrich our current knowledge of probiotics-mediated autophagy in tuberculosis and suggest its implications for innovatively managing tuberculosis.

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来源期刊
CiteScore
10.60
自引率
0.00%
发文量
29
审稿时长
1 months
期刊介绍: Medical Microbiology and Immunology (MMIM) publishes key findings on all aspects of the interrelationship between infectious agents and the immune system of their hosts. The journal´s main focus is original research work on intrinsic, innate or adaptive immune responses to viral, bacterial, fungal and parasitic (protozoan and helminthic) infections and on the virulence of the respective infectious pathogens. MMIM covers basic, translational as well as clinical research in infectious diseases and infectious disease immunology. Basic research using cell cultures, organoid, and animal models are welcome, provided that the models have a clinical correlate and address a relevant medical question. The journal also considers manuscripts on the epidemiology of infectious diseases, including the emergence and epidemic spreading of pathogens and the development of resistance to anti-infective therapies, and on novel vaccines and other innovative measurements of prevention. The following categories of manuscripts will not be considered for publication in MMIM: submissions of preliminary work, of merely descriptive data sets without investigation of mechanisms or of limited global interest, manuscripts on existing or novel anti-infective compounds, which focus on pharmaceutical or pharmacological aspects of the drugs, manuscripts on existing or modified vaccines, unless they report on experimental or clinical efficacy studies or provide new immunological information on their mode of action, manuscripts on the diagnostics of infectious diseases, unless they offer a novel concept to solve a pending diagnostic problem, case reports or case series, unless they are embedded in a study that focuses on the anti-infectious immune response and/or on the virulence of a pathogen.
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