4.6 Article

The response of cecal microbiota to inflammatory state induced by Salmonella enterica serovar Enteritidis

期刊

FRONTIERS IN MICROBIOLOGY
卷 13, 期 -, 页码 -

出版社

FRONTIERS MEDIA SA
DOI: 10.3389/fmicb.2022.963678

关键词

chicken; Salmonella; inflammatory state; transcriptome; microbiome

资金

  1. National Natural Science Foundation of China
  2. National Key Research and Development Program of China
  3. Shandong Modern Agricultural Industry and Technology System
  4. Shandong Provincial Natural Science Foundation
  5. [31601980]
  6. [31872343]
  7. [2021YFD1300102]
  8. [SDAIT-11-02]
  9. [ZR2018MC026]

向作者/读者索取更多资源

This study investigated the response of the cecal microbiota to an inflammatory state caused by Salmonella enterica serovar Enteritidis infection. It was found that the infection improved microbial diversity and promoted microbiota evolution. Some intestinal microorganisms were found to thrive in an inflamed environment, while the overall function of the cecal microbiome was to maintain homeostasis through the up-regulation of microbial metabolism pathways. The infection of S. Enteritidis was closely related to multiple inflammation-related genes and S. Enteritidis was able to compete with symbiotic bacteria.
By combining the experiments of reciprocal crosses of chicken infected with Salmonella enterica serovar Enteritidis (S. Enteritidis), we focused on the common response of cecal microbiota to an inflammatory state in respect of transcriptome and microbiome. The inoculation of S. Enteritidis improved the microbial diversity and promoted the microbiota evolution in our infection model. Correlation analysis between bacteria and inflammation-related genes showed that some intestinal microorganisms were inflammophile and thrived in an inflamed environment. The global function of cecal microbiome was to maintain the homeostasis likely by the up-regulation of microbial metabolism pathway in bacitracin, putrescine, and flavonoids production, although the bacitracin may affect the symbiotic bacteria Enterococcus. The action of S. Enteritidis had close relationships with multiple inflammation-related genes, including the genes PTAFR, LY96, and ACOD1 which proteins are related to the binding and tolerance of LPS, and the genes IL-18, IL-18R1 and IL-18RAP which products can form a functional complex and transmit IL-18 pro-inflammatory signal. Additionally, the infection of S. Enteritidis aroused the transcription of EXFABP, which protein has a potential to sequestrate the siderophore and might cause the decline of Escherichia-Shigella and Enterococcus. S. Enteritidis can escape from the sequestrating through the salmochelin, another kind of siderophore which cannot be recognized by EXFABP. Probably by this way, S. Enteritidis competed with the symbiotic bacteria and edged out the niches. Our research can help to understand the interplay between host, pathogen, and symbiotic bacteria.

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