Lentivirus expressing soluble ST2 alleviates bleomycin-induced pulmonary fibrosis in mice

Gao, Qiaoyan; Li, Yan; Pan, X.; Yuan, Xianli; Xiao, Peng; Li, Mingcai

doi:10.1016/j.intimp.2015.11.015

Cited by 23 publications

(25 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Specifically, it has been documented that IL-33 and BLM result in synergistic effects on pulmonary fibrosis in vivo ( 6 ). In detail, mIL-33 production is induced in macrophages by BLM ( 6 , 20 , 21 , 23 ). Subsequently, IL-33 enhances the polarization of macrophages toward an M2 phenotype ( 6 , 79 , 80 ).…”

Section: Il-33/st2 Axis In Pulmonary Fibrosismentioning

confidence: 99%

“…IL-33 is also elevated in the bleomycin (BLM)-induced murine model of lung injury and fibrosis ( 20 , 21 , 23 ). The lungs of BLM-treated mice showed a substantial accumulation of IL-33-positive cells ( 20 , 21 , 23 ). Specifically, it has been documented that IL-33 and BLM result in synergistic effects on pulmonary fibrosis in vivo ( 6 ).…”

Section: Il-33/st2 Axis In Pulmonary Fibrosismentioning

confidence: 99%

“…Mature forms of IL-33 have been reported to drive production of extremely high levels of Th2 cytokines such as IL-13 ( 80 ). Furthermore, M2 macrophages are polarized by IL-13, and they further promote a Th2 reaction through the IL-13 and the transforming growth factor β (TGF-β) production, vice versa ( 20 – 23 ).…”

Section: Il-33/st2 Axis In Pulmonary Fibrosismentioning

confidence: 99%

See 2 more Smart Citations

IL-33/ST2 Axis in Organ Fibrosis

2018

View full text Add to dashboard Cite

Interleukin 33 (IL-33) is highly expressed in barrier sites, acting via the suppression of tumorigenicity 2 receptor (ST2). IL-33/ST2 axis has long been known to play a pivotal role in immunity and cell homeostasis by promoting wound healing and tissue repair. However, it is also involved in the loss of balance between extensive inflammation and tissue regeneration lead to remodeling, the hallmark of fibrosis. The aim of the current review is to critically evaluate the available evidence regarding the role of the IL-33/ST2 axis in organ fibrosis. The role of the axis in tissue remodeling is better understood considering its crucial role reported in organ development and regeneration. Generally, the IL-33/ST2 signaling pathway has mainly anti-inflammatory/anti-proliferative effects; however, chronic tissue injury is responsible for pro-fibrogenetic responses. Regarding pulmonary fibrosis mature IL-33 enhances pro-fibrogenic type 2 cytokine production in an ST2- and macrophage-dependent manner, while full-length IL-33 is also implicated in the pulmonary fibrotic process in an ST2-independent, Th2-independent fashion. In liver fibrosis, evidence indicate that when acute and massive liver damage occurs, the release of IL-33 might act as an activator of tissue-protective mechanisms, while in cases of chronic injury IL-33 plays the role of a hepatic fibrotic factor. IL-33 signaling has also been involved in the pathogenesis of acute and chronic pancreatitis. Moreover, IL-33 could be used as an early marker for ulcer-associated activated fibroblasts and myofibroblast trans-differentiation; thus one cannot rule out its potential role in inflammatory bowel disease-associated fibrosis. Similarly, the upregulation of the IL-33/ST2 axismay contribute to tubular cell injury and fibrosis via epithelial to mesenchymal transition (EMT) of various cell types in the kidneys. Of note, IL-33 exerts a cardioprotective role via ST2 signaling, while soluble ST2 has been demonstrated as a marker of myocardial fibrosis. Finally, IL-33 is a crucial cytokine in skin pathology responsible for abnormal fibroblast proliferation, leukocyte infiltration and morphologic differentiation of human endothelial cells. Overall, emerging data support a novel contribution of the IL-33/ST2 pathway in tissue fibrosis and highlight the significant role of the Th2 pattern of immune response in the pathophysiology of organ fibrosis.

show abstract

Section: Il-33/st2 Axis In Pulmonary Fibrosismentioning

confidence: 99%

Section: Il-33/st2 Axis In Pulmonary Fibrosismentioning

confidence: 99%

Section: Il-33/st2 Axis In Pulmonary Fibrosismentioning

confidence: 99%

See 1 more Smart Citation

IL-33/ST2 Axis in Organ Fibrosis

2018

View full text Add to dashboard Cite

show abstract

“…Furthermore, intranasal administration of lentiviral expressing soluble ST2 significantly attenuated pulmonary fibrotic change and improved survival rate [80]. A variety of studies have revealed that IL-33 overexpression is implicated in the development of cutaneous fibrotic diseases, such as cutaneous fibrosis [81], psoriasis [82], and progressive systemic sclerosis [83].…”

Section: Uncontrolled Wound Healing Responses: the Role Of Il-33 In Fmentioning

confidence: 99%

Wounds that heal and wounds that don’t − The role of the IL-33/ST2 pathway in tissue repair and tumorigenesis

Millar

O'Donnell

McInnes

et al. 2017

Seminars in Cell & Developmental Biology

View full text Add to dashboard Cite

“…In response to bleomycin challenge, mice show a substantial accumulation of IL-33-positive cells in the lung and full-length IL-33 can potentiate bleomycin-induced inflammation and fibrosis, potentially by upregulating expression of TGF-β and other non-Th2 cytokines [ 139 ]. A subsequent study demonstrated that intratracheal instillation of lentivirus expressing soluble ST2 significantly attenuated pulmonary inflammatory cell infiltration and fibrotic changes and markedly reduced the levels of inflammatory cytokines and TGF-β1 in BAL in mice challenged with bleomycin [ 140 ]. Li et al demonstrated that ST2-deficient mice have attenuated bleomycin-induced lung fibrosis, and this phenomenon could be recreated by IL-33 neutralising antibody treatment [ 141 ].…”

Section: Introductionmentioning

confidence: 99%

The IL-1 cytokine family and its role in inflammation and fibrosis in the lung

2016

View full text Add to dashboard Cite

The IL-1 cytokine family comprises 11 members (7 ligands with agonist activity, 3 receptor antagonists and 1 anti-inflammatory cytokine) and is recognised as a key mediator of inflammation and fibrosis in multiple tissues including the lung. IL-1 targeted therapies have been successfully employed to treat a range of inflammatory conditions such as rheumatoid arthritis and gouty arthritis. This review will introduce the members of the IL-1 cytokine family, briefly discuss the cellular origins and cellular targets and provide an overview of the role of these molecules in inflammation and fibrosis in the lung.

show abstract

Lentivirus expressing soluble ST2 alleviates bleomycin-induced pulmonary fibrosis in mice

Cited by 23 publications

References 28 publications

IL-33/ST2 Axis in Organ Fibrosis

IL-33/ST2 Axis in Organ Fibrosis

Wounds that heal and wounds that don’t − The role of the IL-33/ST2 pathway in tissue repair and tumorigenesis

The IL-1 cytokine family and its role in inflammation and fibrosis in the lung

Contact Info

Product

Resources

About