We suggest a novel modality in terms of IL-25/IL-33/TSLP's pro-fibrotic role in IPF. First, IL-25/IL-33/TSLP fully activates (myo)fibroblasts in fibroblastic foci (FF) in a paracrine-dependent manner. (IL-25/IL-33/TSLP)alveolar epithelial cells-(IL-25R/IL-33R/TSLPR) (myo)fibroblasts axis may contribute greatly to the abnormal epithelial-mesenchymal crosstalk and lung fibrosis. Second, IL-25/IL-33/TSLP causes significant injury and phenotypic changes of alveolar epithelial cells in an autocrine-dependent manner. By acting directly on the two most important cells in the fibrotic process, i.e. alveolar epithelial cells and (myo)fibroblasts, we support the notion that biological therapies targeting IL-25/IL-33/TSLP will shed new light on the cure of IPF patients.
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http://dx.doi.org/10.1177/1535370220915428 | DOI Listing |
Int J Mol Sci
March 2025
Department of Regenerative Medicine, School of Pharmaceutical Sciences, Jilin University, Changchun 130021, China.
Acute lung injury (ALI) is a life-threatening condition triggered by pneumonia, viral infections, or physical trauma. It manifests clinically as progressive respiratory failure and refractory hypoxemia. Using a lipopolysaccharide (LPS)-induced acute lung injury mouse model, we demonstrated that amniotic mesenchymal stem cells (AMSCs) exhibit robust reparative and anti-inflammatory properties.
View Article and Find Full Text PDFActa Crystallogr E Crystallogr Commun
March 2025
Department of PG Studies and Research in Physics Albert Einstein Block UCS Tumkur University, Tumkur Karnataka-572103 India.
The title compound, CHNO, was synthesized by S2 reaction of bromo-methyl coumarin with 4,4-di-methyl-piperidine-2,6-dione. The mol-ecule crystalizes in the monoclinic system with space group 2/. The coumarin unit is almost planar with a dihedral angle between the aromatic rings of 0.
View Article and Find Full Text PDFFront Cell Infect Microbiol
March 2025
Research and Innovation Unit, Health University of Applied Sciences Tyrol, FH Gesundheit Tirol, Innsbruck, Austria.
Introduction: The lung environment is defined by unique biological boundary conditions, including complex alveolar geometry, extracellular matrix composition and mechanical forces generated during respiration. These factors were shown to regulate alveolar permeability, surfactant secretion, cell contractility and apoptosis, but their role in fungal infections remains unknown. is a critical fungal pathogen that causes severe pulmonary infections in immunocompromised individuals.
View Article and Find Full Text PDFThe most common cause of death due to COVID-19 remains respiratory failure. Yet, our understanding of the precise cellular and molecular changes underlying lung alveolar damage is limited. Here, we integrate single cell transcriptomic data of COVID-19 and donor lung tissue with spatial transcriptomic data stratifying histopathological stages of diffuse alveolar damage.
View Article and Find Full Text PDFFront Med (Lausanne)
February 2025
Department of Diving and Hyperbaric Medicine, Naval Medical Center, Shanghai, China.
Objective: There is evidence showing both necroptosis and activation of renin-angiotensin system (RAS) are involved in the pathogenesis of hyperbaric hyperoxic lung injury (HLI). This study aimed to investigate whether RAS activation can induce lung cell necroptosis and the cell specificity of necroptosis in the lung in case of hyperbaric HLI.
Methods: Male SD rats were randomly assigned into control group ( = 12), HLI group ( = 18), captopril group ( = 18), and valsartan group ( = 18).
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