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The systemic inflammation response index as a significant predictor of short-term adverse outcomes in acute decompensated heart failure patients: a cohort study from Southern China.
Front Endocrinol (Lausanne)
January 2025
Jiangxi Cardiovascular Research Institute, Jiangxi Provincial People's Hospital, The First Affiliated Hospital of Nanchang Medical College, Nanchang, Jiangxi, China.
Objective: The deterioration of acute decompensated heart failure (ADHF) is associated with abnormal activation of inflammatory pathways. This study aims to evaluate the impact and predictive value of a novel inflammatory marker, the systemic inflammation response index (SIRI), on short-term adverse outcomes in ADHF patients.
Methods: This retrospective cohort study included 1,448 ADHF patients from Jiangxi Provincial People's Hospital between 2019-2022.
Phagocytic clearance of apoptotic cancer cells (efferocytosis) by tumor-associated macrophages (TAMs) contributes in a substantial manner to the establishment of an immunosuppressive tumor microenvironment. This puts in context our observation that the female steroid hormone 17β-estradiol (E2) facilitates tumor immune resistance through cancer cell extrinsic Estrogen Receptor (ERalpha;) signaling in TAMs. Notable was the finding that E2 induces the expression of CX3CR1 in TAMs to enable efferocytosis of apoptotic cancer cells which results in the suppression of type I interferon (IFN) signaling.
View Article and Find Full Text PDFConnexin 43 and Pannexin 1 hemichannels as endogenous regulators of innate immunity in sepsis.
Front Immunol
January 2025
The Feinstein Institutes for Medical Research, Northwell Health, Manhasset, NY, United States.
Sepsis is a life-threatening organ dysfunction resulting from a dysregulated host response to infections that is initiated by the body's innate immune system. Nearly a decade ago, we discovered that bacterial lipopolysaccharide (LPS) and serum amyloid A (SAA) upregulated Connexin 43 (Cx43) and Pannexin 1 (Panx1) hemichannels in macrophages. When overexpressed, these hemichannels contribute to sepsis pathogenesis by promoting ATP efflux, which intensifies the double-stranded RNA-activated protein kinase R (PKR)-dependent inflammasome activation, pyroptosis, and the release of pathogenic damage-associated molecular pattern (DAMP) molecules, such as HMGB1.
View Article and Find Full Text PDFEnhancing oncolytic virotherapy by extracellular vesicle mediated microRNA reprograming of the tumour microenvironment.
Front Immunol
January 2025
Leeds Institute of Medical Research, School of Medicine, University of Leeds, St. James University Hospital, Leeds, United Kingdom.
Background: There has been limited success of cancer immunotherapies in the treatment of ovarian cancer (OvCa) to date, largely due to the immunosuppressive tumour microenvironment (TME). Tumour-associated macrophages (TAMs) are a major component of both the primary tumour and malignant ascites, promoting tumour growth, angiogenesis, metastasis, chemotherapy resistance and immunosuppression. Differential microRNA (miRNA) profiles have been implicated in the plasticity of TAMs.
View Article and Find Full Text PDFMetabolic adaptation of myeloid cells in the glioblastoma microenvironment.
Front Immunol
January 2025
Aix-Marseille Univ, CNRS, INP, Inst Neurophysiopathol, GlioME Team, Marseille, France.
In recent decades, immunometabolism in cancers has emerged as an interesting target for treatment development. Indeed, the tumor microenvironment (TME) unique characteristics such as hypoxia and limitation of nutrients availability lead to a switch in metabolic pathways in both tumor and TME cells in order to support their adaptation and grow. Glioblastoma (GBM), the most frequent and aggressive primary brain tumor in adults, has been extensively studied in multiple aspects regarding its immune population, but research focused on immunometabolism remains limited.
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