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Staphylococcus aureus vesicles impair cutaneous wound healing through p38 MAPK-MerTK cleavage-mediated inhibition of macrophage efferocytosis.
Cell Commun Signal
January 2025
School of Pharmaceutical Sciences, Southern Medical University, Guangzhou, 510515, China.
Background: Staphylococcus aureus, a known contributor to non-healing wounds, releases vesicles (SAVs) that influence the delicate balance of host-pathogen interactions. Efferocytosis, a process by which macrophages clear apoptotic cells, plays a key role in successful wound healing. However, the precise impact of SAVs on wound repair and efferocytosis remains unknown.
View Article and Find Full Text PDFTandem kinase proteins across the plant kingdom.
Nat Genet
January 2025
Institute of Evolution, University of Haifa, Haifa, Israel.
Plant pathogens pose a continuous threat to global food production. Recent discoveries in plant immunity research unveiled a unique protein family characterized by an unusual resistance protein structure that combines two kinase domains. This study demonstrates the widespread occurrence of tandem kinase proteins (TKPs) across the plant kingdom.
View Article and Find Full Text PDFZika and Dengue Virus Autoimmunity: An Overview of Related Disorders and Their Potential Mechanisms.
Rev Med Virol
January 2025
Department of Critical Care Medicine, Affiliated Hospital of Jiangnan University, Wuxi, China.
Zika virus (ZIKV) and dengue virus (DENV) are two major mosquito-borne flaviviruses that pose a significant threat to the global public health system, particularly in tropical regions. The clinical outcomes related to these viral pathogens can vary from self-limiting asymptomatic infections to various forms of life-threatening pathological conditions such as haemorrhagic disorders. In addition to the direct effects of the viral pathogens, immune processes play also a significant function in the development of diseases mediated by ZIKV and DENV.
View Article and Find Full Text PDFEnterobactin inhibits microbiota-dependent activation of AhR to promote bacterial sepsis in mice.
Nat Microbiol
January 2025
Section of General Surgery, Department of Surgery, University of Chicago, Chicago, IL, USA.
Sepsis is a major cause of morbidity and mortality, but our understanding of the mechanisms underlying survival or susceptibility is limited. Here, as pathogens often subvert host defence mechanisms, we hypothesized that this might influence the outcome of sepsis. We used microbiota analysis, faecal microbiota transplantation, antibiotic treatment and caecal metabolite analysis to show that gut-microbiota-derived tryptophan metabolites including indoles increased host survival in a mouse model of Serratia marcescens sepsis.
View Article and Find Full Text PDFβ-Glucan reprograms neutrophils to promote disease tolerance against influenza A virus.
Nat Immunol
January 2025
Department of Medicine, Department of Pathology, Department of Microbiology & Immunology, McGill University Health Centre, McGill International TB Centre, Meakins Christie Laboratories, McGill University, Montréal, Québec, Canada.
Disease tolerance is an evolutionarily conserved host defense strategy that preserves tissue integrity and physiology without affecting pathogen load. Unlike host resistance, the mechanisms underlying disease tolerance remain poorly understood. In the present study, we investigated whether an adjuvant (β-glucan) can reprogram innate immunity to provide protection against influenza A virus (IAV) infection.
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