Hackettmccartney6643

Leptospirosis is a prevalent zoonotic disease, caused by bacteria of the genus Leptospira. Leptospirosis frequently leads to hemostatic disturbances, and the severe cases are marked by hemorrhages and low platelet number in circulation, which is associated with the patients' poor outcomes. Nevertheless, Leptospira-platelet interactions remain poorly explored. In this study, we performed a series of in vitro experiments evaluating whether leptospires induce human platelet aggregation, activation, and morphological changes. Platelets were incubated with virulent L. interrogans and the platelet outcomes were assessed by aggregometry, flow cytometry, and scanning and transmission electron microscopy. Our results show that leptospires alone do not induce platelet aggregation and activation, and induce platelet cytotoxic effects instead, by clearly inducing platelet disruption and detachment. We show for the first time that virulent leptospires do interact directly with platelets, an event that could trigger pathophysiological effects during the infection. This study might serve as a basis for the development of novel treatments for the disease.Coral reefs are highly diverse marine ecosystems increasingly threatened on a global scale. The foundation species of reef ecosystems are stony corals that depend on their symbiotic microalgae and bacteria for aspects of their metabolism, immunity, and environmental adaptation. Conversely, the function of viruses in coral biology is less well understood, and we are missing an understanding of the diversity and function of coral viruses, particularly in understudied regions such as the Red Sea. Here we characterized coral-associated viruses using a large metagenomic and metatranscriptomic survey across 101 cnidarian samples from the central Red Sea. While DNA and RNA viral composition was different across coral hosts, biological traits such as coral life history strategy correlated with patterns of viral diversity. Coral holobionts were broadly associated with Mimiviridae and Phycodnaviridae that presumably infect protists and algal cells, respectively. Further, Myoviridae and Siphoviridae presumably target members of the bacterial phyla Actinobacteria, Firmicutes, and Proteobacteria, whereas Hepadnaviridae and Retroviridae might infect the coral host. Genes involved in bacterial virulence and auxiliary metabolic genes were common among the viral sequences, corroborating a contribution of viruses to the holobiont's genetic diversity. Our work provides a first insight into Red Sea coral DNA and RNA viral assemblages and reveals that viral diversity is consistent with global coral virome patterns.Non-alcoholic fatty liver disease (NAFLD) is the most common form of chronic liver disease throughout the world. The relationship between gut microbiota and NAFLD has been extensively investigated. The gut microbiota is involved in the regulation of NAFLD by participating in the fermentation of indigestible food, interacting with the intestinal mucosal immune system, and influencing the intestinal barrier function, leading to signaling alteration. Meanwhile, the microbial metabolites not only affect the signal transduction pathway in the gut but also reach the liver far away from gut. In this review, we focus on the effects of certain key microbial metabolites such as short-chain fatty acids, trimethylamine-N-oxide, bile acids, and endogenous ethanol and indole in NAFLD, and also summarize several potential therapies targeting the gut-liver axis and modulation of gut microbiota metabolites including antibiotics, prebiotics, probiotics, bile acid regulation, and fecal microbiota transplantation. Understanding the complex interactions between microbial metabolites and NAFLD may provide crucial insight into the pathogenesis and treatment of NAFLD.Anaerobic granular sludge comprises of highly organized microorganisms with a sophisticated metabolic network. Such aggregates can withstand storage, temperature fluctuations and changes in the substrate supplied for anaerobic digestion. FR 180204 datasheet However, substrate change leads to long adaptation of granular consortia, creating lags in the reactor operations. To speed up adaptation and increase digestion efficiency, bioaugmentation with a robust consortium can be performed. The computational study described here aims to elucidate the mechanisms of bioaugmenting anaerobic granules, utilizing the current body of knowledge on metabolic and biochemical interactions between bacteria in such aggregates. Using a cDynoMiCs simulation environment, an agent-based model was developed to describe bioaugmentation for adaptation of cellobiose-degrading granular consortium to a lipid-rich feed. Lipolytic bacteria were successfully incorporated in silico to the stable granular consortia after 40 days of simulation. The ratio of cellobiose and the lipid-derivative, oleate, in the feed played key role to ensure augmentation. At 0.5 g/L of both cellobiose and oleate in the feed, a homogeneous stable augmented consortium was formed and converted the given amount of substrate to 10.9 mg/L of methane as a final product of anaerobic digestion. The demonstrated model can be used as a planning tool for anaerobic digestion facilities considering transition of the inoculum to a new type of feed.Autophagy can be utilized by the influenza A virus (IAV) to facilitate its replication. However, whether autophagy is induced at the stage of IAV entry is still unclear. Here, we report that IAV induces autophagy by hemagglutinin (HA) binding to heat shock protein 90AA1 (HSP90AA1) distributed on the cell surface. Virus overlay protein binding assay and pull-down assay indicated that IAV HA bound directly to cell surface HSP90AA1. Knockdown of HSP90AA1 weakened H1N1 infection. Incubation of IAV viral particles with recombinant HSP90AA1 or prior blockade of A549 cells with an anti-HSP90AA1 antibody could inhibit attachment of IAV. Moreover, we found that recombinant HA1 protein binding to cell surface HSP90AA1 was sufficient to induce autophagy through the AKT-MTOR pathway. Our study reveals that the HSP90AA1 on cell surface participates in IAV entry by directing binding to the HA1 subunit of IAV and subsequently induces autophagy.