IL-9 aggravates the development of atherosclerosis in ApoE-/- mice

Zhang, Wencai; Tang, Tingting; Nie, Daan; Wen, Shuang; Jia, Chuan-Lei; Zhu, Zhengfeng; Xia, Ni; Nie, Shaofang; Zhou, Siyu; Jiao, Jiao; Dong, Wei; Lv, Bingjie; Xu, Tongjie; Sun, Bing; Lu, Yang; Li, Yuanyuan; Cheng, Long; Liao, Yuhua; Cheng, Xiang

doi:10.1093/cvr/cvv110

Cited by 66 publications

(38 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…IL-9 has recently been reported as a regulator in the pathogenesis of many inflammatory diseases 29,30 . For example, IL-9 is involved in protective immunity to Trichuris muris infections 31 , promotes Treg activation and prevents excessive cartilage destruction and bone loss in arthritis 32 , and promotes tissue repair by amplifying ILC2 function in helminth-induced lung inflammation 33 .…”

Section: Resultsmentioning

confidence: 99%

“…In lung tissue, IL-9 production was restricted to IL-33-induced ILC2 in physiological or inflammatory conditions 34 . IL-9 induces vascular endothelial adhesion molecule-1 expression on mouse aortic EC and attenuates lung inflammation 29,33,35 . We hypothesized that IL-9 might mediate the ILC2-dependent MLEC protection in sepsis.…”

Section: Resultsmentioning

confidence: 99%

“…We also observed lung EC death, as defined with the positive markers of CD31, Annexin V, and 7-AAD, following sepsis. Recently, IL-9 has been reported to be involved, either beneficially or deleteriously, in the pathogenesis of some diseases related to inflammation 29,30 . ILC2 is the main source of IL-9 in mouse lung tissue in physiological or inflammatory circumstances 24 .…”

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Group 2 innate lymphoid cells protect lung endothelial cells from pyroptosis in sepsis

et al. 2018

View full text Add to dashboard Cite

Group 2 innate lymphoid cells (ILC2) are one of three subgroups of innate lymphoid cells (ILC1, ILC2, and ILC3), and the major ILC population detected in the lungs. The function of ILC2 in the regulation of lung inflammation remains unclear. In the current study, we explored an important role of ILC2 in protecting lung endothelial cell (EC) from pyroptosis in sepsis-induced acute lung inflammation and the underlying mechanism. Using a cecal ligation and puncture (CLP) mouse sepsis model, we demonstrated that IL-33, which is released in response to sepsis, acting through its receptor ST2 mediates ILC2 expansion in the lungs. We further showed that the increased ILC2 in the lungs secrete IL-9, which in turn prevents lung EC from undergoing pyroptosis, a pro-inflammatory cell death form, by attenuating caspase-1 activation. These findings suggest a previously unidentified innate pathway that negatively regulates lung inflammation following sepsis.

show abstract

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Group 2 innate lymphoid cells protect lung endothelial cells from pyroptosis in sepsis

et al. 2018

View full text Add to dashboard Cite

show abstract

“…Various inflammatory cytokines such as interleukin-2 (IL-2), interleukin-6 (IL-6), interleukin-17 (IL-17), tumor necrosis factor-alpha (TNF- α ), and interferon-gamma (IFN- γ ) have been implicated in CAD, and their concentrations have been found to be associated with increased risks in ACS patients [8–13]. Most recently, data have shown that interleukin-9 (IL-9) might mediate inflammatory cell infiltration into atherosclerotic lesions and may also play a role in the atherosclerotic process [14, 15]. …”

Section: Introductionmentioning

confidence: 99%

Serum Cytokine Profile in Relation to the Severity of Coronary Artery Disease

Min

Liu

et al. 2017

BioMed Research International

View full text Add to dashboard Cite

Objectives. To investigate the potential association of a set of serum cytokines with the severity of coronary artery disease (CAD). Methods. A total of 201 patients who underwent coronary angiography for chest discomfort were enrolled. The concentrations of serum IFN-γ, TNF-α, IL-2, IL-4, IL-6, IL-10, IL-9, and IL-17 were determined by xMAP multiplex technology. The CAD severity was assessed by Gensini score (GS). Results. The serum levels of TNF-α, IL-6, IL-9, IL-10, and IL-17 were significantly higher in high GS group (GS ≥ 38.5) than those in low GS group (GS < 38.5). Positive correlations were also found between these cytokines and the severity of CAD. After adjustment for other associated factors, three serum cytokines (IL-6, IL-9, and IL-17) and two clinical risk factors (creatinine and LDL-C) were identified as the independent predictors of increased severity of CAD. ROC curve analysis revealed that the logistic regression risk prediction model had a good performance on predicting CAD severity. Conclusions. Combinatorial analysis of serum cytokines (IL-6, IL-9, and IL-17) with clinical risk factors (creatinine and LDL-C) may contribute to the evaluation of the severity of CAD and may help guide the risk stratification of angina patients, especially in primary health facilities and in the catheter lab resource-limited settings.

show abstract

“…However, our results showed significantly reduced levels of IL-9 in T2DM subjects which correlated positively with renal parameters [93]. In CAD-prone apoE KO mice, IL-9 exerts proatherosclerotic effects by inducing VCAM-1 expression and thereby promoting macrophage infiltration and atherosclerotic plaque formation [99]. In humans, increased levels of IL-9 in atherosclerotic disorders were seen both systemically and within the lesion, suggesting a role for the IL-9/IL-9R axis in the atherosclerotic process, potentially involving IL-17 mediated mechanisms [100].…”

Section: Th9 Cytokines In Dm-cadmentioning

confidence: 98%

Metainflammation in Diabetic Coronary Artery Disease: Emerging Role of Innate and Adaptive Immune Responses

Aravindhan

Madhumitha

2016

Journal of Diabetes Research

View full text Add to dashboard Cite

Globally, noncommunicable chronic diseases such as Type-2 Diabetes Mellitus (T2DM) and Coronary Artery Disease (CAD) are posing a major threat to the world. T2DM is known to potentiate CAD which had led to the coining of a new clinical entity named diabetic CAD (DM-CAD), leading to excessive morbidity and mortality. The synergistic interaction between these two comorbidities is through sterile inflammation which is now being addressed as metabolic inflammation or metainflammation, which plays a pivotal role during both early and late stages of T2DM and also serves as a link between T2DM and CAD. This review summarises the current concepts on the role played by both innate and adaptive immune responses in setting up metainflammation in DM-CAD. More specifically, the role played by innate pattern recognition receptors (PRRs) like Toll-like receptors (TLRs), NOD1-like receptors (NLRs), Rig-1-like receptors (RLRs), and C-type lectin like receptors (CLRs) and metabolic endotoxemia in fuelling metainflammation in DM-CAD would be discussed. Further, the role played by adaptive immune cells (Th1, Th2, Th17, and Th9 cells) in fuelling metainflammation in DM-CAD will also be discussed.

show abstract

IL-9 aggravates the development of atherosclerosis in ApoE-/- mice

Abstract: Our results demonstrated that IL-9 exerted pro-atherosclerotic effects in ApoE-/- mice at least partially by inducing VCAM-1 expression, which mediated inflammatory cell infiltration into atherosclerotic lesions.

Cited by 66 publications

References 37 publications

Group 2 innate lymphoid cells protect lung endothelial cells from pyroptosis in sepsis

Group 2 innate lymphoid cells protect lung endothelial cells from pyroptosis in sepsis

Serum Cytokine Profile in Relation to the Severity of Coronary Artery Disease

Metainflammation in Diabetic Coronary Artery Disease: Emerging Role of Innate and Adaptive Immune Responses

Contact Info

Product

Resources

About