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敲除 sHSP 基因决定了植物乳杆菌益生菌特性的一些改变。

Knock out of sHSP genes determines some modifications in the probiotic attitude of Lactiplantibacillus plantarum.

机构信息

SAFE Department, University of Foggia, Via Napoli 25, 71122, Foggia, Italy.

Institute of Sciences of Food Production, National Research Council (CNR) of Italy, c/o CS-DAT, Via Michele Protano, 71121, Foggia, Italy.

出版信息

Biotechnol Lett. 2021 Mar;43(3):645-654. doi: 10.1007/s10529-020-03041-6. Epub 2020 Nov 6.

DOI:10.1007/s10529-020-03041-6
PMID:33156458
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7872990/
Abstract

OBJECTIVE

We investigated whether the knock out of small heat shock protein (sHSP) genes (hsp1, hsp2 and hsp3) impact on probiotic features of Lactiplantibacillus plantarum WCFS1, aiming to find specific microbial effectors involved in microbe-host interplay.

RESULTS

The probiotic properties of L. plantarum WCFS1 wild type, hsp1, hsp2 and hsp3 mutant clones were evaluated and compared through in vitro trials. Oro-gastro-intestinal assays pointed to significantly lower survival for hsp1 and hsp2 mutants under stomach-like conditions, and for hsp3 mutant under intestinal stress. Adhesion to human enterocyte-like cells was similar for all clones, though the hsp2 mutant exhibited higher adhesiveness. L. plantarum cells attenuated the transcriptional induction of pro-inflammatory cytokines on lipopolysaccharide-treated human macrophages, with some exception for the hsp1 mutant. Intriguingly, this clone also induced a higher IL10/IL12 ratio, which is assumed to indicate the anti-inflammatory potential of probiotics.

CONCLUSIONS

sHSP genes deletion determined some differences in gut stress resistance, cellular adhesion and immuno-modulation, also implying effects on in vivo interaction with the host. HSP1 might contribute to immunomodulatory mechanisms, though additional experiments are necessary to test this feature.

摘要

目的

我们研究了敲除小热休克蛋白(sHSP)基因(hsp1、hsp2 和 hsp3)是否会影响植物乳杆菌 WCFS1 的益生菌特性,旨在寻找参与微生物-宿主相互作用的特定微生物效应子。

结果

通过体外试验评估和比较了植物乳杆菌 WCFS1 野生型、hsp1、hsp2 和 hsp3 突变克隆的益生菌特性。口腔-胃肠试验表明,hsp1 和 hsp2 突变体在胃样条件下以及 hsp3 突变体在肠道应激下的存活率显著降低。所有克隆的黏附到人类肠上皮样细胞的能力相似,尽管 hsp2 突变体表现出更高的黏附性。植物乳杆菌细胞减轻了脂多糖处理的人巨噬细胞中促炎细胞因子的转录诱导,hsp1 突变体除外。有趣的是,该克隆还诱导了更高的 IL10/IL12 比值,这被认为表明了益生菌的抗炎潜力。

结论

sHSP 基因缺失导致肠道应激抗性、细胞黏附和免疫调节方面存在一些差异,这也暗示了对与宿主体内相互作用的影响。HSP1 可能有助于免疫调节机制,但需要进一步的实验来验证这一特征。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d845/7872990/0217e31f06b1/10529_2020_3041_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d845/7872990/26c10f346ebb/10529_2020_3041_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d845/7872990/9a6e9aefb968/10529_2020_3041_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d845/7872990/3b14ed735031/10529_2020_3041_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d845/7872990/0217e31f06b1/10529_2020_3041_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d845/7872990/26c10f346ebb/10529_2020_3041_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d845/7872990/9a6e9aefb968/10529_2020_3041_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d845/7872990/3b14ed735031/10529_2020_3041_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d845/7872990/0217e31f06b1/10529_2020_3041_Fig4_HTML.jpg

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