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PhoP/PhoQ双组分系统促成新生小鼠中由[具体因素未给出]诱导的肠道炎症。

PhoP/PhoQ Two-Component System Contributes to Intestinal Inflammation Induced by in Neonatal Mice.

作者信息

Ma Yan, Zhang Yingying, Wang Yuting, Qiao Zhu, Liu Yingying, Xia Xiaodong

机构信息

School of Biological and Food Processing Engineering, Huanghuai University, Zhumadian 463000, China.

The College of Life Sciences, Northwest University, Xi'an 710068, China.

出版信息

Foods. 2024 Sep 4;13(17):2808. doi: 10.3390/foods13172808.

DOI:10.3390/foods13172808
PMID:39272573
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11394756/
Abstract

() is a foodborne pathogen capable of causing severe infections in newborns. The PhoP/PhoQ two-component system exerts a significant influence on bacterial virulence. This study aimed to investigate the impact of the PhoP/PhoQ system on intestinal inflammation in neonatal mice induced by . Neonatal mice were infected orally by BAA-894 (WT), a -gene-deletion strain (Δ), and a complementation strain (Δ), and the intestinal inflammation in the mice was monitored. Deletion of the gene reduced the viable count of in the ileum and alleviated intestinal tissue damage. Moreover, caspase-3 activity in the ileum of the WT- and Δ-infected mice was significantly elevated compared to that of the Δ and control groups. ELISA results showed elevated levels of TNF-α and IL-6 in the ileum of the mice infected with WT and Δ. In addition, deletion of the gene in resulted in a down-regulation of inflammatory genes (IL-1β, TNF-α, IL-6, NF-κB p65, TLR4) within the ileum and decreased inflammation by modulating the TLR4/NF-κB pathway. It is suggested that targeting the PhoP/PhoQ two-component system could be a potential strategy for mitigating -induced neonatal infections.

摘要

()是一种食源性病原体,能够在新生儿中引起严重感染。PhoP/PhoQ双组分系统对细菌毒力有重大影响。本研究旨在探讨PhoP/PhoQ系统对由(此处原文缺失具体病原体名称)诱导的新生小鼠肠道炎症的影响。新生小鼠经口感染BAA - 894(野生型)、一种(此处原文缺失具体基因名称)基因缺失菌株(Δ)和一种互补菌株(Δ),并监测小鼠的肠道炎症。(此处原文缺失具体基因名称)基因的缺失降低了回肠中(此处原文缺失具体病原体名称)的活菌数,并减轻了肠道组织损伤。此外,与Δ和对照组相比,野生型和Δ感染小鼠回肠中的caspase - 3活性显著升高。ELISA结果显示,感染野生型和Δ的小鼠回肠中TNF -α和IL - 6水平升高。此外,(此处原文缺失具体病原体名称)中(此处原文缺失具体基因名称)基因的缺失导致回肠内炎症基因(IL - 1β、TNF -α、IL - 6、NF -κB p65、TLR4)下调,并通过调节TLR4/NF -κB途径减轻炎症。提示靶向PhoP/PhoQ双组分系统可能是减轻(此处原文缺失具体病原体名称)诱导的新生儿感染的潜在策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8d8/11394756/71f027ade989/foods-13-02808-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8d8/11394756/7d3074b19304/foods-13-02808-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8d8/11394756/a0d9095318aa/foods-13-02808-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8d8/11394756/5f85efe9be5a/foods-13-02808-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8d8/11394756/fb834306ae66/foods-13-02808-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8d8/11394756/103761fb7160/foods-13-02808-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8d8/11394756/fe9767e4a83e/foods-13-02808-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8d8/11394756/13e338256a37/foods-13-02808-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8d8/11394756/71f027ade989/foods-13-02808-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8d8/11394756/7d3074b19304/foods-13-02808-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8d8/11394756/a0d9095318aa/foods-13-02808-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8d8/11394756/5f85efe9be5a/foods-13-02808-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8d8/11394756/fb834306ae66/foods-13-02808-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8d8/11394756/103761fb7160/foods-13-02808-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8d8/11394756/fe9767e4a83e/foods-13-02808-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8d8/11394756/13e338256a37/foods-13-02808-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e8d8/11394756/71f027ade989/foods-13-02808-g008.jpg

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