Yanan Peng’s research while affiliated with Shandong Agricultural University and other places

Salmonella enterica serovar Enteritidis (S. Enteritidis) is a common zoonotic pathogen that not only causes gastroenteritis or death of livestock and poultry but also poses a serious threat to human health, causing severe economic losses to the poultry industry and society. Herein, RNA-sequencing (RNA-seq) was used to analyze the transcriptome variation of chicken cecum at four different time points (1, 3, 7, and 14 days) following S. Enteritidis infection. There were 529, 1477, 476, and 432 differentially expressed genes (DEGs) in the cecum at four different days post-infection (dpi), respectively. The DEGs were significantly enriched in various immune-related pathways on 3 dpi and 7 dpi, such as cytokine-cytokine-receptor interaction and Toll-like receptor signaling pathway. DEGs were significantly enriched in several metabolic pathways on 14 dpi. Gene ontology (GO) enrichment of DEGs showed that up-regulated genes were significantly enriched in immune-related terms on 3 and 7 dpi. On 14 dpi, up-regulated genes were mainly enriched in the signaling-related terms, while the down-regulated genes were primarily enriched in the metabolic-related terms. Based on weighted gene co-expression network analysis (WGCNA), the key modules related to energy, non-coding processes, immunity, and development-related functions were identified at 1, 3, 7, and 14 dpi, respectively, and 5, 8, 6, and 5 hub genes were screened out, respectively. This study demonstrated that the chicken cecal transcriptome regulation responding to S. Enteritidis infection is time-dependent. The regulation of S. Enteritidis infection in chickens is coordinated by multiple systems, mainly involving immunity, metabolism, and signal transduction. Both 3 and 7 dpi are key time points for immune response. As the infection progresses, metabolism-related pathways were increasingly identified. This change reflects the dynamic adjustment between immune response and metabolism in Jining Bairi chickens following S. Enteritidis infection. These results suggested that starting from 3 dpi, the chickens gradually transition from an immune response triggered by S. Enteritidis infection to a state where they adapt to the infection by modulating their metabolism.

Salmonella enterica serovar Enteritidis (S. Enteritidis) can colonize in the intestinal tract of chickens and transmit to humans. In order to decrypt the mechanism of avian resistance to S. Enteritidis, we utilized two China local chicken breeds to generate the reciprocal crosses (the Cross and the Reverse‐cross). The two lines of hybrids were orally inoculated with S. Enteritidis at 2‐day old and sampled at 3 days post‐inoculation. Along the analysis direction of multi‐omics, differential metabolites, functional pathways and correlated microbes, we found that 12 species of microbes thrived upon S. Enteritidis challenge and probably contributed to the intestinal stability in the Cross by enhancing the production of phenylpropanoids. Our findings can help to understand the symbiotic and resistant mechanisms derived from the intestinal microbiota.

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.