Comparative Evaluation of the Antimicrobial and Mucus Induction Properties of Selected Strains against Enterotoxigenic .

Probiotics have been shown to bind to host receptors, which are important for pathogen adhesion and induce the host's production of defence factors. They can activate the goblet-cell-derived production of mucins, a major component of the mucus layer and a physical barrier participating in limiting the proximity of microorganisms to the epithelial layer. In the last decade, spp.

Host-Targeted Therapeutics against Multidrug Resistant Intracellular .

is a facultative intracellular pathogen that invades and replicates within many types of human cells. has shown to rapidly overcome traditional antibiotherapy by developing multidrug resistance. Furthermore, intracellular is protected from the last-resort antibiotics-vancomycin, daptomycin, and linezolid-as they are unable to achieve plasma concentrations sufficient for intracellular killing.

Mycoredoxins Are Required for Redox Homeostasis and Intracellular Survival in the Actinobacterial Pathogen .

is a facultative intracellular pathogen that can survive within macrophages of a wide variety of hosts, including immunosuppressed humans. Current antibiotherapy is often ineffective, and novel therapeutic strategies are urgently needed to tackle infections caused by this pathogen. In this study, we identified three mycoredoxin-encoding genes () in the genome of , and we investigated their role in virulence.

Identification of novel targets for host-directed therapeutics against intracellular Staphylococcus aureus.

During patient colonization, Staphylococcus aureus is able to invade and proliferate within human cells to evade the immune system and last resort drugs such as vancomycin. Hijacking specific host molecular factors and/or pathways is necessary for pathogens to successfully establish an intracellular infection. In this study, we employed an unbiased shRNA screening coupled with ultra-fast sequencing to screen 16,000 human genes during S.

Intracellular Elicits the Production of Host Very Long-Chain Saturated Fatty Acids with Antimicrobial Activity.

As a facultative intracellular pathogen, is able to invade and proliferate within many types of mammalian cells. Intracellular bacterial replication relies on host nutrient supplies and, therefore, cell metabolism is closely bound to intracellular infection. Here, we investigated how invasion affects the host membrane-bound fatty acids.

Host-directed kinase inhibitors act as novel therapies against intracellular Staphylococcus aureus.

Host-directed therapeutics are a promising anti-infective strategy against intracellular bacterial pathogens. Repurposing host-targeted drugs approved by the FDA in the US, the MHRA in the UK and/or regulatory equivalents in other countries, is particularly interesting because these drugs are commercially available, safe doses are documented and they have been already approved for other clinical purposes. In this study, we aimed to identify novel therapies against intracellular Staphylococcus aureus, an opportunistic pathogen that is able to exploit host molecular and metabolic pathways to support its own intracellular survival.

Acetaminophen cytotoxicity in HepG2 cells is associated with a decoupling of glycolysis from the TCA cycle, loss of NADPH production, and suppression of anabolism.

Acetaminophen (APAP) is one of the most commonly used analgesics worldwide, and overdoses are associated with lactic acidosis, hepatocyte toxicity, and acute liver failure due to oxidative stress and mitochondrial dysfunction. Hepatoma cell lines typically lack the CYP450 activity to generate the reactive metabolite of APAP observed in vivo, but are still subject to APAP cytotoxicity. In this study, we employed metabolic profiling and isotope labelling approaches to investigate the metabolic impact of acute exposure to cytotoxic doses of APAP on the widely used HepG2 cell model.

Intracellular Staphylococcus aureus Modulates Host Central Carbon Metabolism To Activate Autophagy.

is a facultative intracellular pathogen that invades and replicates within many types of phagocytic and nonphagocytic cells. During intracellular infection, is capable of subverting xenophagy and escaping to the cytosol of the host cell. Furthermore, drug-induced autophagy facilitates the intracellular replication of , but the reasons behind this are unclear.