Neutrophils are the first barriers for resisting the invasion, proliferation, and damage caused by Salmonella Typhimurium. However, the mechanisms that control this resistance are not completely understood. In this study, we established an in vitro Salmonella infection model in porcine neutrophils, and analyzed the cellular transcriptome by deep sequencing and flow cytometry. The results showed that ribosomal gene transcription was inhibited, and two of these genes, RPL39 and RPL9, were related to TRP53 activation. Furthermore, several important innate immunity genes were also inhibited. Knock-down of RPL39 and RPL9 by siRNA caused an approximate fourfold up-regulation of TRP53. Knock-down of RPL39 and RPL9 also resulted in a significant down-regulation of IFNG and TNF, indicating an inhibition of the innate immune response. Silencing of RPL39 and RPL9 also resulted in the up-regulation of FAS, RB1, CASP6, and GADD45A, which play roles in cell cycle arrest and apoptosis. Neutrophils were either first treated with RPL39 siRNA, RPL9 siRNA, TRP53 activator, or TRP53 inhibitor, and then infected with Salmonella. Knock-down of RPL39 and RPL9, or treatment with TRP53 activator, can increase the intracellular proliferation of Salmonella in neutrophils. We speculate that much of the Salmonella virulence can be attributed to the enhancement of cell cycle arrest and the inhibition of the innate immune response, which allows the bacteria to successfully proliferate intracellularly.

Angiotensin-converting enzyme 2 (ACE2) has been identified as the key receptor of SARS coronavirus that plays a key role in the pathogenesis of SARS. It is known that ACE2 mRNA can be expressed in most organs. However, the protein expression of ACE2 is not clear yet. To explore the role of ACE2 as a precipitating factor in digestive organ damage under COVID-19, this study investigated the expression of ACE2 protein in the human liver, esophagus, stomach, and colon. The result showed that ACE2 can be expressed in the liver, esophagus, stomach, and colon, which suggests SARS-CoV-2 may enter the digestive system through ACE2 and cause liver and gastrointestinal damage. It is hoped that the result of the study will provide a new strategy for the prevention and treatment of digestive organ damage under COVID-19.

Background: With increasing research on Alzheimer's disease and periodontitis, many studies suggest a close correlation between Alzheimer's disease and periodontitis, but the underlying pathophysiological mechanisms remain unclear. The aim of this study was to identify potential pivotal genes and pathways associated with both diseases by using a bioinformatics approach. Materials/Methods: The GEO dataset GSE5281 for Alzheimer's disease patients and normal controls was downloaded from the GEO database. The GSE10334 dataset for periodontitis patients and healthy controls was also obtained. Differentially expressed genes (DEGs) for the Alzheimer's disease and periodontitis datasets were obtained, as well as genes common between them. Further GO and KEGG enrichment analyses were performed on the common genes. To determine the pathogenesis associated with Alzheimer's disease and periodontitis, protein-protein interaction (PPI) networks were constructed. Finally, the diagnostic value of HUB genes in the Alzheimer's disease and periodontitis datasets was analyzed separately using SPSS software. Results: A total of 16 common genes were obtained for Alzheimer's disease and periodontitis with a P value <0.05. 7 GO entries and 2 KEGG pathways were obtained. In addition, the first 6 central genes (CD4, KDR, CXCR4, CXCL12, JAK2 and PTPN11) were selected with a P<0.05. Conclusion: The results of this study suggest that some novel genes play an important role in the development and progression of Alzheimer's disease and periodontitis. More experimental studies and clinical trials are needed to validate our results.