M2 Macrophage‐Derived Extracellular Vesicles Reprogram Immature Neutrophils into Anxa1hi Neutrophils to Enhance Inflamed Bone Regeneration DOI Creative Commons

Yufei Yao,

Yijia Yin, Fangyuan Shuai

et al.

Advanced Science, Journal Year: 2025, Volume and Issue: unknown

Published: April 25, 2025

Abstract Periodontitis is a microbiome‐related inflammation that can lead to irreversible bone reduction and even tooth loss. This study reveals macrophage polarization states significantly influence periodontal homeostasis, with M2 macrophage‐derived extracellular vesicles (M2‐EVs) playing pivotal role in mitigating periodontitis‐induced Single‐cell RNA sequencing of tissues treated M2‐EVs uncovered unique Anxa1 hi neutrophil subpopulation exhibiting pro‐reparative properties. characterized by immaturity demonstrated osteogenic angiogenic capabilities vivo, partially mediated through the secretion oncostatin M (OSM) signals. The findings suggest this functional heterogeneity arises from disrupting maturation trajectory, reprogramming genes, such as Acvrl1 Fpr2 , driving differentiation reparative subpopulation. work underscores potential targeting macrophage‐neutrophil interactions promote regeneration inflamed tissues.

Language: Английский

Secondary Neutropenias DOI Creative Commons
Alister C. Ward

Biomedicines, Journal Year: 2025, Volume and Issue: 13(2), P. 497 - 497

Published: Feb. 17, 2025

Neutrophils are a critical component of immunity, particularly against bacteria and other pathogens, but also in inflammation tissue repair. As consequence, individuals with neutropenia, defined by reduction absolute neutrophil counts, exhibit strong propensity to severe infections that typically present muted symptoms. Neutropenias encompass heterogeneous set disorders, comprising primary neutropenias, which specific genes mutated, the more common secondary have diverse non-genetic causes. These include hematological cancers, involving both direct effects cancer itself indirect impacts via chemotherapeutic, biological agents cell-based approaches used for treatment. Other significant causes neutropenias non-chemotherapeutic drugs, autoimmune immune diseases, nutrient deficiencies. collectively act impacting production bone marrow and/or destruction throughout body. This review describes clinical manifestations detailing their underlying management, discussion alternative emerging therapeutic approaches.

Language: Английский

Citations

0

The role of KLF4 in phagocyte activation during infectious diseases DOI Creative Commons
Toni Herta,

Aritra Bhattacharyya,

Stefan Hippenstiel

et al.

Frontiers in Immunology, Journal Year: 2025, Volume and Issue: 16

Published: April 16, 2025

Phagocytes, including granulocytes (especially neutrophils), monocytes, macrophages, and dendritic cells, are essential components of the innate immune system, bridging adaptive immunity. Their activation function tightly regulated by transcription factors that coordinate responses. Among these, Krüppel-like factor 4 (KLF4) has gained attention as a regulator phagocyte differentiation, polarization, inflammatory modulation. However, its role is highly context-dependent, exhibiting both pro- anti-inflammatory properties based on environmental signals, cellular states, invading pathogen. KLF4 influences monocyte-to-macrophage differentiation shapes macrophage promoting either or regulatory phenotypes depending external cues. In neutrophils, it affects reactive oxygen species production activation, while in regulates monocyte-to-dendritic cell cytokine secretion. Its diverse involvements responses suggests contributes to maintaining balance between effective pathogen defense prevention excessive potentially harmful inflammation. This review summarizes current knowledge phagocytes during infections, highlighting mechanisms, context-dependent roles, impact resolution. Additionally, potential implications for therapeutic interventions targeting discussed.

Language: Английский

Citations

0

Clca1 Deficiency Exacerbates Colitis Susceptibility via Impairment of Mucus Barrier Integrity and Gut Microbiota Homeostasis DOI
Zhi Liu, Hong Zhang, Jing Jing Wang

et al.

Microbiological Research, Journal Year: 2025, Volume and Issue: unknown, P. 128191 - 128191

Published: April 1, 2025

Language: Английский

Citations

0

Vascular Remodeling: The Multicellular Mechanisms of Pulmonary Hypertension DOI Open Access

Jinjin Dai,

H Chen,

Jiayi Fang

et al.

International Journal of Molecular Sciences, Journal Year: 2025, Volume and Issue: 26(9), P. 4265 - 4265

Published: April 30, 2025

Pulmonary hypertension (PH) is a serious cardiovascular disease caused by variety of pathogenic factors, which characterized increased pulmonary vascular resistance (PVR) and progressive elevation mean artery pressure (mPAP). This can lead to right ventricular hypertrophy and, in severe cases, heart failure even death. Vascular remodeling—a pathological modification involving aberrant vasoconstriction, cell proliferation, apoptosis resistance, inflammation the system—is significant hallmark PH critical process its progression. Recent studies have found that remodeling involves participation diversity cellular alterations, such as dysfunction endothelial cells (PAECs), proliferation migration smooth muscle (PASMCs), phenotypic differentiation fibroblasts, inflammatory response immune cells, pericyte proliferation. review focuses on mechanisms intercellular crosstalk these process, emphasizing recent advances knowledge regarding signaling pathways, responses, apoptosis, To develop better treatments, list possible therapeutic approaches meant slow down certain biological functions provided, with aim providing new insights into treatment simplifying intricacies complex connections. In this review, comprehensive academic databases PubMed, Embase, Web Science, Google Scholar were systematically searched discuss relevant human animal PH, focus PH.

Language: Английский

Citations

0

The recombinant spike S1 protein induces injury and inflammation in co-cultures of human alveolar epithelial cells and macrophages DOI Creative Commons
Yanru Liu,

Hong Yu,

Jia He

et al.

PLoS ONE, Journal Year: 2025, Volume and Issue: 20(2), P. e0318881 - e0318881

Published: Feb. 10, 2025

The current lack of a straightforward and convenient modeling approach to simulate the onset acute lung injury (ALI) has impeded fundamental research hindered screening therapeutic drugs in coronavirus disease 2019 (COVID-19). co-cultured human pulmonary alveolar epithelial cells (HPAEpics) macrophages (AMs) were exposed complete medium, three concentrations recombinant spike S1 protein (0.1, 1, 10 μg/mL), or lipopolysaccharide (LPS) (10 μg/mL). harvested at 2, 3 days post-exposure. Lactate dehydrogenase (LDH) release, IL-6, TNF-ɑ, malondialdehyde (MDA) production quantified compared. Compared those co-cultures HPAEpics AMs concentration μg/mL demonstrated significantly increased levels LDH release (22.9% vs. 9.1%, 25.7%), IL-6 (129 74, 110 pg/mg protein), TNF-ɑ (75 51, 86 protein) production, similar LPS. However, no statistically significant differences observed MDA production. 1 2 post-exposure, post-exposure exhibited (23.4% 14.9%, 16.7%), (127 81, 97 (5.6 3.2, 3.8 nmol/mg but lower (58 79 than After exposure, showed (25.3% 18.4%), (5.5 4.3 compared monocultures, 13.8%), (139 98 4.7 decreased (59 95 monocultures. Conclusions: exposure induced inflammation This methodology for establishing COVID-19-associated ALI model may have promising potential applications value.

Language: Английский

Citations

0

Coordination of Neutrophil and Apoptosis-Inducing Ligand in Inflammatory Diseases DOI Creative Commons
Hanyu Xue,

Ran Xie,

Zhiwei Wang

et al.

Journal of Inflammation Research, Journal Year: 2025, Volume and Issue: Volume 18, P. 3607 - 3621

Published: March 1, 2025

Abstract: As the most abundant innate immune cells, neutrophils play a key role in host's anti-infective activity and tissue damage/repair process of sterile inflammation. Due to restriction apoptosis other regulatory mechanisms, have short survival time vivo. Because death domain cytoplasmic regions, some members tumor necrosis factor receptor superfamily (TNFRSF) are defined as receptors, such TNFR-I, Fas DR4/DR5. TNF-α, FasL TRAIL, which known apoptosis-inducing ligand, can bind receptors activate intracellular pathways induce apoptosis. Accumulating studies found that these three ligands an important system by coordinating with neutrophil, including neutrophil recruitment/infiltration function performing. In this review, we summarize existing targeting diagnosis treatment for diseases, focus on involvement regulated inflammatory diseases under current cognition. Keywords: infectious inflammation, inflammation

Language: Английский

Citations

0

Multi-omics integration and machine learning identify and validate neutrophil extracellular trap-associated gene signatures in chronic rhinosinusitis with nasal polyps DOI
Fu Shu, Yaping Wang, Linglong Li

et al.

Clinical Immunology, Journal Year: 2025, Volume and Issue: 275, P. 110473 - 110473

Published: March 13, 2025

Language: Английский

Citations

0

M2 Macrophage‐Derived Extracellular Vesicles Reprogram Immature Neutrophils into Anxa1hi Neutrophils to Enhance Inflamed Bone Regeneration DOI Creative Commons

Yufei Yao,

Yijia Yin, Fangyuan Shuai

et al.

Advanced Science, Journal Year: 2025, Volume and Issue: unknown

Published: April 25, 2025

Abstract Periodontitis is a microbiome‐related inflammation that can lead to irreversible bone reduction and even tooth loss. This study reveals macrophage polarization states significantly influence periodontal homeostasis, with M2 macrophage‐derived extracellular vesicles (M2‐EVs) playing pivotal role in mitigating periodontitis‐induced Single‐cell RNA sequencing of tissues treated M2‐EVs uncovered unique Anxa1 hi neutrophil subpopulation exhibiting pro‐reparative properties. characterized by immaturity demonstrated osteogenic angiogenic capabilities vivo, partially mediated through the secretion oncostatin M (OSM) signals. The findings suggest this functional heterogeneity arises from disrupting maturation trajectory, reprogramming genes, such as Acvrl1 Fpr2 , driving differentiation reparative subpopulation. work underscores potential targeting macrophage‐neutrophil interactions promote regeneration inflamed tissues.

Language: Английский

Citations

0