Interleukin-35 inhibits lipopolysaccharide-induced endothelial cell activation by downregulating inflammation and apoptosis

Li, Meng; Liu, Yue; Fu, Yang Xin; Gong, Ren; Xia, Huasong; Huang, Xiao

doi:10.1016/j.yexcr.2021.112784

Cited by 19 publications

(7 citation statements)

References 39 publications

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“…This current study verified that IL-35 treatment can reduce the production of ROS, TXNIP, and p38 MAPK expression. Consistent with our results, IL-35 has been shown to inhibit the LPS-induced EC activation via inhibition of the MAPK signaling pathway (19).…”

Section: Discussionsupporting

confidence: 92%

“…IL-35, an anti-inflammatory and antioxidant cytokine, has a protective effect against vascular EC damage (18). For example, in the mouse sepsis model, IL-35 has been shown to inhibit lipopolysaccharide-induced EC activation via the mitogen-activated proliferation protein kinase (MAPK)-activated protein 1 (AP-1)-mediated inflammatory pathway (19). Moreover, in apolipoprotein E (ApoE) knockout mice, IL-35 inhibited EC activation induced by lysophosphatidylcholine via reducing the production of mitochondrial ROS, thereby inhibiting the development of atherosclerotic lesions (20).…”

Section: Original Articlementioning

confidence: 99%

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Interleukin-35 attenuates blood-brain barrier dysfunction caused by cerebral ischemia-reperfusion injury through inhibiting brain endothelial cell injury

Qian¹,

Li²,

Lin³

et al. 2022

Ann Transl Med

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Background: , an anti-inflammatory and antioxidant cytokine, plays a potent immunosuppressive role in various diseases. However, the effects of IL-35 on blood-brain barrier (BBB) dysfunction in ischemic stroke are not well characterized.Methods: A total of 150 male C57BL/6 mice (aged 6-8 weeks and weighing 20-25 g) were used in this study. The protective effects of IL-35 against BBB dysfunction were examined using a mouse model of middle cerebral artery occlusion (MCAO) and an in vitro model of oxygen-glucose deprivation/reoxygenation (OGD/R) injury in mouse brain endothelial cells (bEnd.3).Results: Intracerebroventricular administration of IL-35 (10 μg/g) was found to reduce cerebral edema and Evans blue (EB) leakage, and increase the expression of tight junction (TJ) proteins, thereby attenuating MCAO-induced neurological deficit in mice. Moreover, IL-35 (20 ng/mL) treatment upregulated the expression of TJ proteins in OGD/R-induced bEnd.3 cells. IL-35 also markedly suppressed the expression of caspase-1, IL-1β, and gasdermin D (GSDMD) in vivo and in vitro. In addition, IL-35 decreased the generation of reactive oxygen species (ROS) and inhibited the expression of thioredoxin-interacting protein (TXNIP) in OGD/R-induced bEnd.3 cells.Conclusions: These results indicated that IL-35 exerts a protective effect on the BBB by targeting the ROS/TXNIP/caspase-1 pathway in cerebral ischemia-reperfusion (I/R) injury.

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Section: Discussionsupporting

confidence: 92%

Section: Original Articlementioning

confidence: 99%

Interleukin-35 attenuates blood-brain barrier dysfunction caused by cerebral ischemia-reperfusion injury through inhibiting brain endothelial cell injury

Qian¹,

Li²,

Lin³

et al. 2022

Ann Transl Med

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“…Some of these seven genes have played important roles in LC. Signal transducer and activator of transcription 1 (STAT1) regulates cellular responses to IFNs, cytokines and growth factors ( 14 ). Moreover, it was reported that KHSRP promoted cell invasion and metastasis by activating the STAT1 signaling pathway in LC ( 15 ).…”

Section: Discussionmentioning

confidence: 99%

Development and validation of a novel M1 macrophage-related gene prognostic signature for lung cancer

Zhu¹,

Liu²,

Mao³

et al. 2023

J Thorac Dis

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Background: Lung cancer (LC) is the most common cancer. Using data from The Cancer Genome Atlas (TCGA), we analyzed the functional roles of M1 macrophage status in LC patients.Methods: Clinical and transcriptome data of LC patients were obtained from the TCGA dataset.We identified M1 macrophage-related genes in LC patients and investigated the underlying molecular mechanisms of these genes in LC patients. After performing a least absolute shrinkage and selection operator (LASSO) Cox regression analysis, the LC patients were divided into two subtypes, and the underlying mechanism of the association between them was further explored. A comparison of immune infiltration was conducted between the two subtypes. Based on gene set enrichment analysis (GSEA), the key regulators associated with subtypes were further explored.Results: M1 macrophage-related genes were identified using TCGA data, and these genes might be related to the activation of the immune response and cytokine-mediated signaling pathways in LC. A seven M1 macrophage-related gene signature (including STAT1, TAP1, UBE2L6, TAP2, CXCR6, PSMB8 and CD2) was identified in LC using LASSO Cox regression analysis. Two subtypes (low risk and high risk) of LC patients were created based on the seven M1 macrophage-related gene signature. Univariate and multivariate survival analyses further confirmed that the subtype classification was an effective independent prognostic factor.Moreover, the two subtypes were correlated with immune infiltration, and GSEA revealed that the pathways of tumor cell proliferation and immune-related biological processes (BPs) might play an important role in LC in the high-risk group and low-risk group, respectively.Conclusions: M1 macrophage-related subtypes of LC were identified and were closely associated with immune infiltration. The gene signature involved in M1 macrophage-related genes could help make a distinction and predict prognosis for LC patients.

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“…IL-35, which belongs to the IL-12 cytokine family, is regarded as a novel immune-suppressive cytokine (149). IL-35 may alleviate disease states by inhibiting pulmonary endothelial proliferation, apoptosis, and activation (133,150). IL-35 treatment has been proven to prevent murine TRALI via inhibition of endothelial activation (133), which could provide new insights into therapeutic targets.…”

Section: Targeting Endothelial Activationmentioning

confidence: 99%

Update on transfusion-related acute lung injury: an overview of its pathogenesis and management

Lian

2023

Front. Immunol.

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Transfusion-related acute lung injury (TRALI) is a severe adverse event and a leading cause of transfusion-associated death. Its poor associated prognosis is due, in large part, to the current dearth of effective therapeutic strategies. Hence, an urgent need exists for effective management strategies for the prevention and treatment of associated lung edema. Recently, various preclinical and clinical studies have advanced the current knowledge regarding TRALI pathogenesis. In fact, the application of this knowledge to patient management has successfully decreased TRALI-associated morbidity. This article reviews the most relevant data and recent progress related to TRALI pathogenesis. Based on the existing two-hit theory, a novel three-step pathogenesis model composed of a priming step, pulmonary reaction, and effector phase is postulated to explain the process of TRALI. TRALI pathogenesis stage-specific management strategies based on clinical studies and preclinical models are summarized with an explication of their models of prevention and experimental drugs. The primary aim of this review is to provide useful insights regarding the underlying pathogenesis of TRALI to inform the development of preventive or therapeutic alternatives.

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Interleukin-35 inhibits lipopolysaccharide-induced endothelial cell activation by downregulating inflammation and apoptosis

Cited by 19 publications

References 39 publications

Interleukin-35 attenuates blood-brain barrier dysfunction caused by cerebral ischemia-reperfusion injury through inhibiting brain endothelial cell injury

Interleukin-35 attenuates blood-brain barrier dysfunction caused by cerebral ischemia-reperfusion injury through inhibiting brain endothelial cell injury

Development and validation of a novel M1 macrophage-related gene prognostic signature for lung cancer

Update on transfusion-related acute lung injury: an overview of its pathogenesis and management

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