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Extensive studies have shown that potassium diformate (KDF), an antibiotic substitute used as a feed additive, improves animal growth performance, although there is less direct evidence of its preventive effect on bacterial infections and its influence on the intestinal flora of animals. In this study, the inhibition effect of KDF on Salmonella enterica serovar Pullorum, an important enteric pathogen causing pullorum disease, was investigated in vitro and on a chicken infection model. The effect of KDF on the diversities and structures of chicken duodenal and cecum flora were also investigated using 16S rRNA gene sequencing. The results showed that addition of 0.5% KDF in feed or 0.1% KDF in drinking water significantly reduced the bacterial loads and the degree of pathological changes in the cecum, improved digestion and reduced the pH of the gastrointestinal tract of chickens infected with S. pullorum. KDF also significantly modified the diversity and abundance of intestinal microflorae in chickens. In particular, it promoted the colonization of several probiotics, such as Bacteroides, Blautia, Ruminococcus_torques_group and Faecalibacteriumm, which are involved in maintenance of the intestinal barrier, modulation of inflammation, energy supply for intestinal cells and pathogen resistance. These results enrich the theoretical basis for the clinical application of KDF in chickens. [ABSTRACT FROM AUTHOR]

The Gram-negative bacterium Actinobacillus pleuropneumoniae is the etiologic agent of porcine contagious pleuropneumoniae, a lethal respiratory infectious disease causing great economic losses in the swine industry worldwide. In order to better interpret the genetic background of serotypic diversity, nine genomes of A. pleuropneumoniae reference strains of serovars 1, 2, 4, 6, 9, 10, 11, 12, and 13 were sequenced by using rapid high-throughput approach. Based on 12 genomes of corresponding serovar reference strains including three publicly available complete genomes (serovars 3, 5b, and 7) of this bacterium, we performed a comprehensive analysis of comparative genomics and first reported a global genomic characterization for this pathogen. Clustering of 26,012 predicted protein-coding genes showed that the pan genome of A. pleuropneumoniae consists of 3,303 gene clusters, which contain 1,709 core genome genes, 822 distributed genes, and 772 strain-specific genes. The genome components involved in the biogenesis of capsular polysaccharide and lipopolysaccharide O antigen relative to serovar diversity were compared, and their genetic diversity was depicted. Our findings shed more light on genomic features associated with serovar diversity of A. pleuropneumoniae and provide broader insight into both pathogenesis research and clinical/epidemiological application against the severe disease caused by this swine pathogen. doi: 10.1128/JB.00535-10

Arctigenin (ACT) is a novel anti‐inflammatory lignan extracted from Arctium lappa L, a herb commonly used in traditional Chinese herbal medicine. In this study, we investigated the molecular mechanism whereby ACT inhibits PCV2 infection‐induced proinflammatory cytokine production in vitro and in vivo. We observed that in PCV2 infection+ACT treated PK‐15 cells, proinflammatory cytokine production was significantly reduced, compared to the PCV2‐infected cells. The transfection and luciferase reporter assay confirmed that ACT suppressed NF‐κB signalling pathway activation following PCV2 infection in PK‐15 cells. Furthermore, western blotting demonstrated that ACT suppressed the NF‐κB signal pathway in PCV2 infection‐stimulated PK‐15 cells by inhibiting the translocation of p65 from the cytoplasm to the nucleus and IκBα phosphorylation. BALB/c mice were used as a model to evaluate the anti‐inflammatory effect of ACT in vivo. We found that the BALB/c mice inoculated with PCV2 infection + ACT treated showed a significant reduction of proinflammatory cytokine production in serum, lung and spleen tissue, compared to the PCV2‐infected mice. Western blotting confirmed that ACT suppressed the NF‐κB signal pathway in PCV2‐infected mice by inhibiting the translocation of p65 from the cytoplasm to the nucleus and IκBα phosphorylation in lung tissue. Our studies first demonstrate that ACT inhibits PCV2 infection‐induced proinflammatory cytokine production by suppressing the phosphorylation and nuclear translocation of NF‐κB in vitro and in vivo. These results will help further develop ACT as a Traditional Chinese herbal medicine remedy in the treatment of porcine circovirus‐associated diseases. This study investigates the molecular mechanism of ACT inhibits PCV2 infection‐induced proinflammatory cytokine production in vitro and in vivo. The results demonstrate that ACT could inhibit PCV2 infection‐induced proinflammatory cytokine production by suppressing the phosphorylation and nuclear translocation of NF‐κB. This study will help further develop ACT as a Traditional Chinese herbal medicine remedy in the treatment of PCVADs. [ABSTRACT FROM AUTHOR]

This article analyses business transitions among Chinese immigrant entrepreneurs in France during the Covid-19 pandemic. Drawing on a historical overview of the development of ethnic Chinese businesses over the last century and an empirical study carried out in five different industrial sectors (import and export, retail, catering, hotel, and tobacco) of the French economy, we examine what challenges these entrepreneurs have faced during the pandemic, what strategies they have adopted in response to these challenges, and what has enabled them to shift business patterns and commercial practices in this unprecedented situation. Our findings show that the Covid-19 pandemic has accelerated the transition of Chinese immigrant entrepreneurship in France, from offline operations to digital business. However, the pandemic may not be the direct cause of this business transition; rather, it has created unique conditions which facilitate the transition. Before the pandemic, some Chinese entrepreneurs had already made or partially made the transition to "integrating online and offline businesses," "hiring beyond Chinese ethnic networks," and "paying attention to the local country's policy directions," which helped them greatly reduce the negative impacts of the pandemic. During the pandemic, two unprecedented business opportunities were opened up: "fostering local production" and "seeking low-risk sectors," which some Chinese entrepreneurs have proactively pursued since April/May 2020. These may be the new trends for Chinese entrepreneurs in France in the future. Theoretically, our study suggests that business transitions among Chinese entrepreneurs in France need to be examined beyond the framework of pure economic rationality, taking into consideration the intersection of new dynamics of Chinese migration into host country and the cross-cultural, cross-institutional, cross-thinking, and cross-border social engagement of the entrepreneurs themselves before, during, and after the pandemic. 摘要: 本文分析了新冠疫情期间在法华裔企业家的商业转型。通过对上个世纪华裔企业发展的历史回顾，以及在法国经济中的五个不同产业部门（进出口、零售、餐饮、酒店和烟草）进行的实证研究，我们考察了这些企业家在疫情期间所面临的挑战，他们为应对挑战而采取的策略，以及他们能在这些前所未有的挑战下成功转变商业模式的原因。我们的研究结果表明，新冠疫情加速了法国华裔移民企业家的商业转型，例如从线下经营转向数字化经营。然而，疫情可能并非这些商业转型的直接原因，而是为转型创造了独特的条件，促进了转型。在疫情发生之前，一些华裔企业家已经实现或部分实现了"线上线下业务融合"、"在华人族裔网络之外招工"、"关注移入国本地政策导向"等商业转型，这帮助他们大大降低了新冠疫情带来的负面影响。疫情同时也为他们带来了两个前所未有的商机:"促进本地生产"和"寻求低风险行业"。这是 2020 年 4–5 月以来一些华商的商业动向，也可能是未来中国企业家在法国发展的新趋势。在理论层面，我们的研究表明，考察在法华商的商业转型需要跳出纯经济理性的分析框架，去全盘分析华人移民与移入国的互动新动态，以及华裔企业家在新冠疫情前、中、后的跨文化、跨机构、跨思维、跨国界的社会参与。 [ABSTRACT FROM AUTHOR]

This article focuses on the discrimination and racism experienced by Chinese migrants and their descendants during the Covid-19 pandemic. It analyses this group's increasing awareness and activism toward racial discrimination in French society. The paper is based on an empirical investigation using qualitative and quantitative research methods (online surveys and interviews) with people of Chinese origin living in France. In addition, qualitative data from news media and activists is also crucial to this study because of the important role they play in the social construction of the anti-racism movement. This study shows that the Covid-19 pandemic highlights how the discrimination and racism experienced by people of Chinese origin can take various forms. The epidemic has become a catalyst for Chinese immigration to resist racism, especially among descendants, and among more recent and highly-skilled Chinese immigrants, who have broken their silence, united, and participated in a more activist manner. [ABSTRACT FROM AUTHOR]

Pathogenic bacteria have evolved many strategies to evade surveillance and attack by complements. Streptococcus suis is an important zoonotic pathogen that infects humans and pigs. Hyaluronidase (HylA) has been reported to be a potential virulence factor of S. suis. However, in this study, it was discovered that the genomic region encoding HylA of the virulent S. suis strain SC19 and other ST1 strains was truncated into four fragments when aligned with a strain containing intact HylA and possessing hyaluronidase activity. As a result, SC19 had no hyaluronidase activity, but one truncated HylA fragment, designated as HylS,’ directly interacted with complement C3b, as confirmed by western ligand blotting, pull-down, and ELISA assays. The deposition of C3b and membrane attack complex (MAC) formation on the surface of a HylS’-deleted mutant (ΔhylS’) was significantly increased compared to wild-type SC19. In human sera and whole blood, ΔhylS’ survival was significantly reduced compared to that in SC19. The resistance of ΔhylS’ to macrophages and human polymorphonuclear neutrophil PMNs also decreased. In a mouse infection model, ΔhylS’ showed reduced lethality and lower bacterial load in the organs compared to that of SC19. We conclude that the truncated hyaluronidase HylS’ fragment contributes to complement evasion and the pathogenesis of S. suis. [ABSTRACT FROM AUTHOR]

Extraintestinal pathogenic Escherichia coli (ExPEC) is an important zoonotic pathogen. Recently, ExPEC has been reported to be an emerging problem in pig farming. However, the mechanism of pathogenicity of porcine ExPEC remains to be revealed. In this study, we constructed a transposon (Tn) mutagenesis library covering Tn insertion in over 72% of the chromosome-encoded genes of a virulent and multi-drug resistant porcine ExPEC strain PCN033. By using a mouse infection model, a transposon-directed insertion site sequencing (TraDIS) assay was performed to identify in vivo fitness factors. By comparing the Tn insertion frequencies between the input Tn library and the recovered library from different organs, 64 genes were identified to be involved in fitness during systemic infection. 15 genes were selected and individual gene deletion mutants were constructed. The in vivo fitness was evaluated by using a competitive infection assay. Among them, Δ fimG was significantly outcompeted by the WT strain in vivo and showed defective adhesion to host cells. rfa which was involved in lipopolysaccharide biosynthesis was shown to be critical for in vivo fitness which may have resulted from its role in the resistance to serum killing. In addition, several metabolic genes including fepB , sdhC , fepG , gltS , dcuA , ccmH , ddpD , narU , glpD , malM , and yabL and two regulatory genes metJ and baeS were shown as important determinants of in vivo fitness of porcine ExPEC. Collectively, this study performed a genome-wide screening for in vivo fitness factors which will be important for understanding the pathogenicity of porcine ExPEC.

Nitrate metabolism is an adaptation mechanism used by many bacteria for survival in anaerobic environments. As a by-product of inflammation, nitrate is used by the intestinal bacterial pathogens to enable gut infection. However, the responses of bacterial respiratory pathogens to nitrate are less well understood. Actinobacillus pleuropneumoniae is an important bacterial respiratory pathogen of swine. Previous studies have suggested that adaptation of A. pleuropneumoniae to anaerobiosis is important for infection. In this work, A. pleuropneumoniae growth and pathogenesis in response to the nitrate were investigated. Nitrate significantly promoted A. pleuropneumoniae growth under anaerobic conditions in vitro and lethality in mice. By using narQ and narP deletion mutants and single-residue-mutated complementary strains of Δ narQ , the two-component system NarQ/P was confirmed to be critical for nitrate-induced growth, with Arg50 in NarQ as an essential functional residue. Transcriptome analysis showed that nitrate upregulated multiple energy-generating pathways, including nitrate metabolism, mannose and pentose metabolism, and glycerolipid metabolism via the regulation of NarQ/P. Furthermore, narQ , narP , and its target gene encoding the nitrate reductase Nap contributed to the pathogenicity of A. pleuropneumoniae. The Nap inhibitor tungstate significantly reduced the survival of A. pleuropneumoniae in vivo , suggesting that Nap is a potential drug target. These results give new insights into how the respiratory pathogen A. pleuropneumoniae utilizes the alternative electron acceptor nitrate to overcome the hypoxia microenvironment, which can occur in the inflammatory or necrotic infected tissues.

Actinobacillus pleuropneumoniae causes porcine pleuropneumonia. The function of the outer membrane protein W gene ( ompW ) of A. pleuropneumoniae has not been evaluated. Thus a deletion mutant of ompW , Δ ompW , was constructed to explore the effect of ompW gene deletion on bacterial growth, biofilm formation, bacterial morphology, oxidative tolerance, susceptibility to antibiotics, and the expression of ribosome synthesis and ABC transporter related genes. Results showed that the ompW gene deletion did not affect biofilm formation and the growth of A. pleuropneumoniae but did affect bacterial morphology during steady growth, oxidative tolerance, and bacterial susceptibility to polymyxin B, kanamycin, and penicillin. The ompW gene deletion also affected the expression of ribosome synthesis and ABC transporter related genes. These results suggested that ompW may regulate the biological phenotype of A. pleuropneumoniae ., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Chen, Shao, Wu, He, Yang, Chen, Jin, Huang, Lei, Xu, Li, Zhang, Wan, Liu and Zhou.)

Flagellum-mediated bacterial motility is important for bacteria to take up nutrients, adapt to environmental changes, and establish infection. The twin-arginine translocation system (Tat) is an important protein export system, playing a critical role in bacterial physiology and pathogenesis. It has been observed for a long time that the Tat system is critical for bacterial motility. However, the underlying mechanism remains unrevealed. In this study, a comparative transcriptomics analysis was performed with extraintestinal pathogenic Escherichia coli (ExPEC), which identified a considerable number of genes differentially expressed when the Tat system was disrupted. Among them, a large proportion of flagellar biosynthesis genes showed downregulation, indicating that transcription regulation plays an important role in mediating the motility defects. We further identified three Tat substrate proteins, MdoD, AmiA, and AmiC, that were responsible for the nonmotile phenotype. The Rcs system was deleted in the Δ tat , the Δ mdoD , and the Δ amiA Δ amiC strains, which restored the motility of Δ mdoD and partially restored the motility of Δ tat and Δ amiA Δ amiC . The flagella were also observed in all of the Δ tat Δ rcsDB , Δ mdoD Δ rcsDB , and Δ amiA Δ amiC Δ rcsDB strains, but not in the Δ tat , Δ mdoD , and Δ amiA Δ amiC strains, by using transmission electron microscopy. Quantitative reverse transcription-PCR data revealed that the regulons of the Rcs system displayed differential expression in the tat mutant, indicating that the Rcs signaling was activated. Our results suggest that the Rcs system plays an important role in mediating the motility defects of the tat mutant of ExPEC. IMPORTANCE The Tat system is an important protein export system critical for bacterial physiology and pathogenesis. It has been observed for a long time that the Tat system is critical for bacterial motility. However, the underlying mechanism remains unrevealed. In this study, we combine transcriptomics analysis and bacterial genetics, which reveal that transcription regulation plays an important role in mediating the motility defects of the tat mutant of extraintestinal pathogenic Escherichia coli. The Tat substrate proteins responsible for the motility defects are identified. We further show that the Rcs system contributes to the motility suppression. We for the first time reveal the link between the Tat system and bacterial motility, which is important for understanding the physiological functions of the Tat system.

Live bacterial vector vaccines are one of the most promising vaccine types and have the advantages of low cost, flexibility, and good safety. Meanwhile, protein secretion systems have been reported as useful tools to facilitate the release of heterologous antigen proteins from bacterial vectors. The twin-arginine translocation (Tat) system is an important protein export system that transports fully folded proteins in a signal peptide-dependent manner. In this study, we constructed a live vector vaccine using an engineered commensal Escherichia coli strain in which amiA and amiC genes were deleted, resulting in a leaky outer membrane that allows the release of periplasmic proteins to the extracellular environment. The protective antigen proteins SLY, enolase, and Sbp against Streptococcus suis were targeted to the Tat pathway by fusing a Tat signal peptide. Our results showed that by exploiting the Tat pathway and the outer membrane-defective E. coli strain, the antigen proteins were successfully secreted. The strains secreting the antigen proteins were used to vaccinate mice. After S. suis challenge, the vaccinated group showed significantly higher survival and milder clinical symptoms compared with the vector group. Further analysis showed that the mice in the vaccinated group had lower burdens of bacteria load and slighter pathological changes. Our study reports a novel live bacterial vector vaccine that uses the Tat system and provides a new alternative for developing S. suis vaccine.

An avian influenza virus strain, A/pigeon/Hubei/RP25/2012 (H5N1), was isolated from pigeons in Hubei province, China. Phylogenetic analysis indicates that the HA gene belongs to clade 2.3.4 and the other internal genes present different recombination events. Information about the strain provides basic research data for epidemiological evidences for revealing influenza evolution., (Copyright © 2015 Yao et al.)