N2 neutrophils may participate in spontaneous recovery after transient cerebral ischemia by inhibiting ischemic neuron injury in rats

Hou, Yanming; Yang, Depeng; Xiang, Rongwu; Wang, Huiyang; Wang, Xianshi; Zhang, Haotian; Wang, Pengwei; Zhang, Zhen; Che, Xiaohang; Liu, Yinglu; Gao, Yue; Yu, Xiang‐Nan; Gao, Xiaoyun; Zhang, Wen; Yang, Jingyu; Wu, Chunfu

doi:10.1016/j.intimp.2019.105970

Cited by 32 publications

(36 citation statements)

References 57 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Even though a dramatic infiltration of neutrophils was observed in both APAP and BDL groups, the number of MoMFs was only markedly increased in the BDL group (extremely low in the APAP group), implying that the main cell type involved in the inflammatory response is different in APAP- and BDL-induced liver injury (Figure 3I and Figure 4F). Recent evidence suggests that infiltrated neutrophils can polarize into a protective phenotype, which exerts an anti-inflammatory effect and restores homeostasis (55). Here, we verified the existence of protective neutrophil subtype and analyzed the polarization trajectory of neutrophils from Neu1 to Neu3 subtype (Figure 3K and Supplementary Figure S4).…”

Section: Discussionmentioning

confidence: 99%

A single-cell transcriptomic atlas characterizes liver non-parenchymal cells in healthy and diseased mice

Wang

Qian

et al. 2021

Preprint

View full text Add to dashboard Cite

The heterogeneity of liver non-parenchymal cells (NPCs) is essential for liver structure and function. However, the current understanding of liver NPCs, especially in different liver diseases, remains incompletely elucidated. Here, a single-cell transcriptome atlas of 171,814 NPCs from healthy and 5 typical liver disease mouse models, including alcoholic liver disease, nonalcoholic steatohepatitis (NASH), drug-induced liver injury, cholestatic, and ischemia-reperfusion liver injury is constructed. The inter- and intra-group heterogeneity of 12 types (and numerous subtypes) of NPCs involving endothelial cells, hepatic stellate cells (HSCs), neutrophils, T cells, and mononuclear phagocytes (MPs) are summarized. A protective subtype of neutrophils characterized by Chil3high is validated and found significantly increasing only in drug-induced and cholestatic liver injury models. Transcriptional regulatory network analysis reveals disease-specific transcriptional reprogramming. Metabolic activity analysis indicates that fibrosis is accompanied by increases in glycolysis and retinol metabolism in activated HSCs and MPs. Moreover, we found that cell-cell interactions between cholangiocytes and immune cells contribute more to cholestatic liver fibrosis compared with NASH, while HSCs are more important for NASH fibrosis. Our atlas, together with an interactive website provides a systematic view of highly heterogeneous NPCs and a valuable resource to better understand pathological mechanisms underlying liver diseases.

show abstract

Section: Discussionmentioning

confidence: 99%

A single-cell transcriptomic atlas characterizes liver non-parenchymal cells in healthy and diseased mice

Wang

Qian

et al. 2021

Preprint

View full text Add to dashboard Cite

show abstract

“…Interestingly, recent evidence has suggested that neutrophils may adopt an anti-inflammatory phenotype by expressing of Ym1 and CD206 ( 72 ). Accelerated by peroxisome proliferator-activated receptor gamma (PPAR-γ) agonists while being hampered by Toll-like-receptor (TLR) activation, the N2 polarization of neutrophils promoted the engulfment of neutrophils by microglia/macrophages, which led to reductions in brain edema and infarct volume ( 73 , 74 ).…”

Section: Role Of Peripheral Immune Cells In the Disruption Of Bbb In Strokementioning

confidence: 99%

Immune Cells in the BBB Disruption After Acute Ischemic Stroke: Targets for Immune Therapy?

et al. 2021

View full text Add to dashboard Cite

Blood-Brain Barrier (BBB) disruption is an important pathophysiological process of acute ischemic stroke (AIS), resulting in devastating malignant brain edema and hemorrhagic transformation. The rapid activation of immune cells plays a critical role in BBB disruption after ischemic stroke. Infiltrating blood-borne immune cells (neutrophils, monocytes, and T lymphocytes) increase BBB permeability, as they cause microvascular disorder and secrete inflammation-associated molecules. In contrast, they promote BBB repair and angiogenesis in the latter phase of ischemic stroke. The profound immunological effects of cerebral immune cells (microglia, astrocytes, and pericytes) on BBB disruption have been underestimated in ischemic stroke. Post-stroke microglia and astrocytes can adopt both an M1/A1 or M2/A2 phenotype, which influence BBB integrity differently. However, whether pericytes acquire microglia phenotype and exert immunological effects on the BBB remains controversial. Thus, better understanding the inflammatory mechanism underlying BBB disruption can lead to the identification of more promising biological targets to develop treatments that minimize the onset of life-threatening complications and to improve existing treatments in patients. However, early attempts to inhibit the infiltration of circulating immune cells into the brain by blocking adhesion molecules, that were successful in experimental stroke failed in clinical trials. Therefore, new immunoregulatory therapeutic strategies for acute ischemic stroke are desperately warranted. Herein, we highlight the role of circulating and cerebral immune cells in BBB disruption and the crosstalk between them following acute ischemic stroke. Using a robust theoretical background, we discuss potential and effective immunotherapeutic targets to regulate BBB permeability after acute ischemic stroke.

show abstract

“…Interestingly, neutrophils may protect neuron damage against ischemic injury via the anti-inflammatory phenotype N2 expressing Ym1 and CD206 (Hou et al, 2019 ). Neutrophils can reprogram to N2 phenotype in brain inflammation which is modulated by PPAR-γ activation or by TLR activation.…”

Section: The Communication Between Microglia and Cns-infiltrating Cellsmentioning

confidence: 99%

Microglia: The Hub of Intercellular Communication in Ischemic Stroke

Yun-sha

Lian

et al. 2022

Front. Cell. Neurosci.

View full text Add to dashboard Cite

Communication between microglia and other cells has recently been at the forefront of research in central nervous system (CNS) disease. In this review, we provide an overview of the neuroinflammation mediated by microglia, highlight recent studies of crosstalk between microglia and CNS resident and infiltrating cells in the context of ischemic stroke (IS), and discuss how these interactions affect the course of IS. The in-depth exploration of microglia-intercellular communication will be beneficial for therapeutic tools development and clinical translation for stroke control.

show abstract

N2 neutrophils may participate in spontaneous recovery after transient cerebral ischemia by inhibiting ischemic neuron injury in rats

Cited by 32 publications

References 57 publications

A single-cell transcriptomic atlas characterizes liver non-parenchymal cells in healthy and diseased mice

A single-cell transcriptomic atlas characterizes liver non-parenchymal cells in healthy and diseased mice

Immune Cells in the BBB Disruption After Acute Ischemic Stroke: Targets for Immune Therapy?

Microglia: The Hub of Intercellular Communication in Ischemic Stroke

Contact Info

Product

Resources

About