Background: (-)-Epigallocatechin-3-gallate (EGCG), a major component of green tea, has been found to inhibit the influenza virus. However, the mechanism of EGCG anti-influenza virus effect needs to be further explored. Methods: BEAS-2B cells were treated with different concentrations of EGCG or were treated with EGCG for different times. CCK8 assay was used to detect the cell viability, and quantitative real time polymerase chain reaction (qRT-PCR) and enzyme-linked immunosorbent assay were employed to measure the interferon (IFN)-λ2 mRNA and protein expression levels. The phospho-p38 mitogen-activated protein kinase (P-p38 MAPK), phospho-extracellular signal-regulated kinase (P-ERK), and phospho-c-Jun N-terminal kinase (P-JNK) expression were tested by western blot. Then, p38 MAPK, ERK, and JNK inhibitor were used to study the effect of p38 MAPK, ERK, and JNK signaling pathways on IFN-λ2 expression. The BEAS-2B cells were treated with EGCG, EGCG and IFN λ2 neutralizing antibody or control antibody for 12 h, and were infected with influenza A virus (IAV) (H1N1) for 1 h. After 12 h, nucleoprotein (NP) mRNA and protein expression levels of H1N1 were assessed by qRT-PCR and western blot.
Results:The IFN-λ2 mRNA and protein expression levels in BEAS-2B cells were up-regulated after EGCG (treatment in time-and dose-dependent manners the concentration range from 0 to 50 μg/mL had no cytotoxicity). Meanwhile, the P-p38 MAPK, P-ERK, and P-JNK expression levels were up-regulated.IFN-λ2 mRNA and protein expression was inhibited after p38 MAPK inhibitor pre-treatment, but not by ERK and JNK inhibitors. Furthermore, the expression of H1N1 NP gene and protein decreased after EGCG pre-treatment, while IFN-λ2 neutralizing antibody attenuated the effect of EGCG inhibiting the expression of H1N1 NP gene and protein.Conclusions: EGCG inhibited IAV H1N1 by inducing the expression of IFN-λ2 in BEAS-2B cells through the p38 MAPK signaling pathway.
Background and Objective: The distribution of components in the cell membrane is not uniform, but is organized into specific functional microdomains, known as "lipid rafts". These lipid rafts consist of cholesterol, sphingolipids, and various proteins. Studies have shown that lipid rafts contain multiple proteins that are closely related to signal transduction and immune response. Furthermore, lipid rafts are the sites where a variety of pathogens invade the cells, and are associated with the persistent infection of some pathogens, especially Helicobacter pylori (Hp). We are going to explore a new method to treat Hp by discussing the important role of lipid rafts in Hp persistent infection.Methods: Papers on lipid rafts were retrieved to analyze the evolution of the definition of lipid raft, research techniques, and studies on the correlation of lipid rafts with pathogens infecting host cells.
Background: Helicobacter pylori (H. pylori) is a Gram-negative pathogenic bacterium that causes chronic gastritis and other gastric diseases in humans. In Tibet, China, the infection of H. pylori is an important risk factor that caused gastric cancer.Methods: To understand the characteristics of this pathogen in Tibet, five strains of H. pylori were isolated from three patients' oral cavity or stomach who had either a gastric ulcer or gastritis. We performed genome sequences of these five clinical strains on Illumina Hiseq, and 55,016-63666 SNVs/InDels were identified by comparing to the reference strain of H. pylori 26995.
Results:The phylogenetic analysis with multi-locus sequence typing (MLST) showed that five Tibetan strains were defined as hpEurope population and their proteins encoded by the cagA gene also presented a western type. Also, the strains that were isolated from the same patients' oral cavity and stomach exhibited homology in molecular evolution.Conclusions: This is the first study to investigate the phylogenetic population structure of the epidemic strains of H. pylori in Tibet, which may improve cognition of Tibetan strains and confirm the homology of the strains from oral cavity and stomach.
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