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Unlabelled: Crosstalk between autophagy, host cell death, and inflammatory host responses to bacterial pathogens enables effective innate immune responses that limit bacterial growth while minimizing coincidental host damage. ( ) thwarts innate immune defense mechanisms in alveolar macrophages (AMs) during the initial stages of infection and in recruited bone marrow-derived cells during later stages of infection. However, how protective inflammatory responses are achieved during infection and the variation of the response in different macrophage subtypes remain obscure.
View Article and Find Full Text PDFTargeting Protein Kinase C-α Prolongs Survival and Restores Liver Function in Sepsis: Evidence from Preclinical Models.
Pharmacol Res
January 2025
Jena University Hospital, Department of Anesthesiology and Intensive Care Medicine, Friedrich-Schiller-University Jena, Jena, Germany; Jena University Hospital, Center for Sepsis Control and Care, Friedrich-Schiller-University Jena, Jena, Germany; Friedrich-Schiller-University Jena, Faculty of Medicine, Jena, Germany. Electronic address:
Sepsis is a life-threatening organ failure resulting from a poorly regulated infection response. Organ dysfunction includes hepatic involvement, weakening the immune system due to excretory liver failure, and metabolic dysfunction, increasing the death risk. Although experimental studies correlated excretory liver functionality with immune performance and survival rates in sepsis, the proteins and pathways involved remain unclear.
View Article and Find Full Text PDFHost-Directed Therapy in Pandemic Preparedness.
JAMA
January 2025
4th Department of Internal Medicine, National and Kapodistrian University of Athens, Greece.
N-acetylcysteine modulates markers of oxidation, inflammation and infection in tuberculosis.
J Infect
January 2025
The Aurum Institute, Johannesburg, South Africa; Case Western Reserve University, Cleveland USA; Department of Medicine, Vanderbilt University, Nashville USA.
Background: Half the global tuberculosis health burden is due to post-tuberculosis lung disease. Host-directed therapies have been proposed to reduce this burden. N-acetylcysteine (NAC) provides the conditionally essential amino acid cysteine required for synthesis of glutathione, an antioxidant thiol.
View Article and Find Full Text PDFMetformin improves infection by strengthening macrophage antimicrobial functions.
Front Immunol
December 2024
Centre of Molecular Inflammation Research, Department of Molecular and Clinical Medicine, Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology (NTNU), Trondheim, Norway.
Introduction: The incidence and prevalence of infections with non-tuberculous mycobacteria such as (Mav) are increasing. Prolonged drug regimens, inherent antibiotic resistance, and low cure rates underscore the need for improved treatment, which may be achieved by combining standard chemotherapy with drugs targeting the host immune system. Here, we examined if the diabetes type 2 drug metformin could improve Mav-infection.
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