Free Radical Biology and Medicine, Journal Year: 2022, Volume and Issue: 194, P. 12 - 22
Published: Nov. 25, 2022
Language: Английский
Free Radical Biology and Medicine, Journal Year: 2022, Volume and Issue: 194, P. 12 - 22
Published: Nov. 25, 2022
Language: Английский
Signal Transduction and Targeted Therapy, Journal Year: 2024, Volume and Issue: 9(1)
Published: Jan. 17, 2024
The lungs were long thought to be sterile until technical advances uncovered the presence of lung microbial community. microbiome healthy is mainly derived from upper respiratory tract (URT) but also has its own characteristic flora. selection mechanisms in lung, including clearance by coughing, pulmonary macrophages, oscillation cilia, and bacterial inhibition alveolar surfactant, keep transient mobile, which different other organs. bacteriome been intensively studied recently, relatively little research focused on mycobiome virome. This up-to-date review retrospectively summarizes microbiome's history, composition, function. We focus interaction with oropharynx gut emphasize role it plays innate adaptive immune responses. More importantly, we multiple diseases, asthma, chronic obstructive disease (COPD), fibrosis, bronchiectasis, pneumonia. impact coronavirus 2019 (COVID-19) cancer comprehensively studied. Furthermore, summarizing therapeutic potential diseases examining shortcomings field, propose an outlook direction research.
Language: Английский
Citations
126Communications Biology, Journal Year: 2025, Volume and Issue: 8(1)
Published: Jan. 7, 2025
Gram-positive bacterial pneumonia is a significant cause of hospitalization and death. Shortage good experimental model therapeutic targets hinders the cure acute lung injury (ALI). This study has established mouse ALI using bacteria Lactobacillus casie cell wall extracts (LCWE) identified key regulator NLRP3. We show that LCWE induces TNF, NF-κB signaling, so on pathways. Similar to lipopolysaccharide (LPS), infiltration CD11b-positive cells inflammation in lungs. also triggers inflammatory signaling through TLR2, different from LPS TLR4. It suggests cytokines amplify relying NLRP3 LCWE-induced ALI. deletion disrupts inflammation, IL-1β cleavage, neutrophils macrophages injured lung. Our highlights an animal for target prevent damage drives cleaved induced by casei extracts, highlighting its role as pneumonia.
Language: Английский
Citations
3International Immunopharmacology, Journal Year: 2023, Volume and Issue: 125, P. 111161 - 111161
Published: Nov. 9, 2023
Language: Английский
Citations
27Inflammation, Journal Year: 2024, Volume and Issue: 47(4), P. 1067 - 1082
Published: Feb. 3, 2024
Language: Английский
Citations
14Biomedicine & Pharmacotherapy, Journal Year: 2024, Volume and Issue: 175, P. 116773 - 116773
Published: May 21, 2024
Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) represent a significant global burden of morbidity mortality, with being the primary cause death in affected patients. The pathogenesis injury, however, remains complex issue. In recent years, role immune system has attracted extensive attention worldwide. Despite advancements our understanding various subtypes, limitations persist both prevention treatment. This review investigates immunopathogenesis ALI/ARDS, aiming to elucidate pathological processes mediated by dendritic cells (DCs), natural killer (NK) cells, phagocytes, neutrophils. Furthermore, article expounds on critical contributions gut microbiota, inflammatory pathways, cytokine storms development ALI/ARDS.
Language: Английский
Citations
12Journal of Nanobiotechnology, Journal Year: 2024, Volume and Issue: 22(1)
Published: June 8, 2024
Abstract Acute lung injury (ALI) is a life threatening disease in critically ill patients, and characterized by excessive reactive oxygen species (ROS) inflammatory factors levels the lung. Multiple evidences suggest that nanozyme with diversified catalytic capabilities plays vital role this fatal injury. At present, we developed novel class of polydopamine (PDA) coated cerium dioxide (CeO 2 ) (Ce@P) acts as potent ROS scavenger for scavenging intracellular suppressing responses against ALI. Herein, aimed to identify Ce@P combining NIR irradiation could further strengthen its capacity. Specifically, triggered exhibited most antioxidant anti-inflammatory behaviors lipopolysaccharide (LPS) induced macrophages through decreasing levels, down-regulating TNF-α, IL-1β IL-6, up-regulating level cytokine (SOD-2), inducing M2 directional polarization (CD206 up-regulation), increasing expression HSP70. Besides, performed intravenous (IV) injection LPS ALI rat model, found it significantly accumulated tissue 6 h after injection. It was also observed + presented superior inflammation, alleviating diffuse alveolar damage, well promoting repair. All all, has strategy using synergistic enhanced treatment ALI, which can serve promising therapeutic clinical derived diseases well.
Language: Английский
Citations
12Redox Biology, Journal Year: 2024, Volume and Issue: 71, P. 103116 - 103116
Published: March 6, 2024
Oxidative stress plays an important role in the pathogenesis of acute lung injury (ALI). As a typical post-translational modification triggered by oxidative stress, protein S-glutathionylation (PSSG) is regulated redox signaling pathways and diverse roles conditions. In this study, we found that GSTP downregulation exacerbated LPS-induced human epithelial cells mice ALI models, confirming protective effect against both vitro vivo. Additionally, positive correlation was observed between total PSSG level expression tissues. Further results demonstrated inhibited KEAP1-NRF2 interaction promoting process KEAP1. By integration mass spectrometry, molecular docking, site-mutation validation assays, identified C434 KEAP1 as key site catalyzed GSTP, which promoted dissociation complex activated subsequent anti-oxidant genes. vivo experiments with AAV-GSTP confirmed inflammation activating NRF2 downstream antioxidant pathways. Collectively, study revealed novel regulatory mechanism anti-inflammatory function lungs modulating KEAP1/NRF2 pathway. Targeting at manipulation or activity might be promising therapeutic strategy for stress-induced progression.
Language: Английский
Citations
10International Journal of Biological Macromolecules, Journal Year: 2025, Volume and Issue: unknown, P. 139550 - 139550
Published: Jan. 1, 2025
Language: Английский
Citations
2Life, Journal Year: 2025, Volume and Issue: 15(1), P. 88 - 88
Published: Jan. 13, 2025
In this study, the anti-inflammatory effect of hot water extract Endarachne binghamiae (EB-WE), a type marine brown algae, was investigated in LPS-stimulated RAW 264.7 cells and an acute lung injury (ALI) mouse model induced by intranasal LPS administration. Treatment with EB-WE significantly inhibited NO pro-inflammatory cytokine (TNF-a IL-6) production cells. mRNA analysis, expression cytokines, COX-2, iNOS mRNAs, down-regulated treatment. The phosphorylation MAPK, IkB, PI3K/AKT molecules responsible for signal pathways during inflammation macrophages also EB-WE. vivo ALI, oral administration reduced level cytokines (TNF-a, IL-1b, chemokines (MCP-1, CXC-16, CXCL1, TARC) serum or bronchoalveolar lavage fluid (BALF) mice. Similarly to results cells, treatment intracellular mediated tissues mice decreased mRNAs inflammatory mediators such as TNF-a, IL-6, iNOS, COX-2. Furthermore, inhibitory on ALI apparently confirmed histological examination through tissue staining. Taken together, it is clear that has potential activity effectively ameliorate responses down-regulation NF-kB, activation, suppress LPS. These findings strongly suggest promising natural product beneficial developing preventive treatments cures inflammation-related diseases.
Language: Английский
Citations
2RNA Biology, Journal Year: 2025, Volume and Issue: 22(1), P. 1 - 12
Published: March 7, 2025
Acute lung injury (ALI) is a life-threatening condition with high rates of morbidity and mortality. Recently, there has been growing evidence suggesting link between lncRNA HOTAIR ALI. Nonetheless, the precise role mechanism in ALI remain to be fully elucidated. siHOTAIR transfection, qPCR detection (HOTAIR), ELISA (TNF-α, IL-6, IL-1β), Lactate detection, Glucose uptake experiment, Cell Apoptosis Analysis, Fluorescence situ hybridization (FISH) assay. Through we discovered that plays secretion inflammatory factors further regulates glucose metabolism epithelial cells. Moreover, comparison knockdown cells overexpression revealed promotes cellular aerobic sugar metabolism, leading increased cell apoptosis. Our in-depth research also identified an interaction LIN28 protein. Knocking down resulted downregulation protein expression, which subsequently inhibited expression transporter GLUT1. This indicates facilitates boosts glycolysis by modulating protein, thereby promoting inflammation apoptosis acute injury. The findings presented this article offer significant insights into function suggest potential therapeutic target for treatment condition.
Language: Английский
Citations
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