Hu Geng, Liu Liying, Miao Xiuxiu, Zhao Yanan, Peng Yanan, Liu Lewen, Li Xianyao
College of Animal Science and Technology, Shandong Provincial Key Laboratory of Animal Biotechnology and Disease Control and Prevention, Shandong Agricultural University, Tai'an, Shandong, China.
College of Life Sciences, Shandong Agricultural University, Tai'an, Shandong, China.
Front Microbiol. 2022 Aug 25;13:963678. doi: 10.3389/fmicb.2022.963678. eCollection 2022.
By combining the experiments of reciprocal crosses of chicken infected with serovar Enteritidis (. Enteritidis), we focused on the common response of cecal microbiota to an inflammatory state in respect of transcriptome and microbiome. The inoculation of . 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 Enteritidis had close relationships with multiple inflammation-related genes, including the genes , , and which proteins are related to the binding and tolerance of LPS, and the genes and which products can form a functional complex and transmit IL-18 pro-inflammatory signal. Additionally, the infection of Enteritidis aroused the transcription of , which protein has a potential to sequestrate the siderophore and might cause the decline of Escherichia-Shigella and Enterococcus. Enteritidis can escape from the sequestrating through the salmochelin, another kind of siderophore which cannot be recognized by EXFABP. Probably by this way, 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.
通过对感染肠炎血清型鸡的正反交实验进行综合分析，我们聚焦于盲肠微生物群在转录组和微生物组方面对炎症状态的共同反应。在我们的感染模型中，肠炎血清型的接种改善了微生物多样性并促进了微生物群的进化。细菌与炎症相关基因之间的相关性分析表明，一些肠道微生物是“嗜炎菌”，在炎症环境中大量繁殖。盲肠微生物组的整体功能可能是通过上调杆菌肽、腐胺和类黄酮生产中的微生物代谢途径来维持体内平衡，尽管杆菌肽可能会影响共生细菌肠球菌。肠炎血清型的作用与多个炎症相关基因密切相关，包括与LPS结合和耐受性相关的蛋白质的基因、，以及其产物可形成功能复合物并传递IL-18促炎信号的基因和。此外，肠炎血清型的感染引发了的转录，其蛋白质有可能螯合铁载体，并可能导致大肠杆菌-志贺氏菌属和肠球菌数量下降。肠炎血清型可以通过另一种铁载体沙门菌素逃脱螯合，沙门菌素不能被EXFABP识别。肠炎血清型可能通过这种方式与共生细菌竞争并排挤其生态位。我们的研究有助于理解宿主、病原体和共生细菌之间的相互作用。
