ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2011
An essential role for Stat3 in regulating IgG immune complex-induced pulmonary inflammation.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 25 citations in OpenAlex.
- Protective effect of liriodendrin on IgG immune complex-induced acute lung injury via inhibiting SRC/STAT3/MAPK signaling pathway: a network pharmacology research.Naunyn-Schmiedeberg's archives of pharmacology · 2023Article
- IgG immune complex-induced acute lung injury is ameliorated by cAMP via down-regulation of C/EBP- and AP-1-mediated transcriptions.Journal of inflammation (London, England) · 2023Article
- Xuanfei Baidu Decoction suppresses complement overactivation and ameliorates IgG immune complex-induced acute lung injury by inhibiting JAK2/STAT3/SOCS3 and NF-κB signaling pathway.Phytomedicine : international journal of phytotherapy and phytopharmacology · 2023Article
- Suppressing STAT3 activity protects the endothelial barrier from VEGF-mediated vascular permeability.Disease models & mechanisms · 2021Article
- The Crucial Role of PPARγ-Egr-1-Pro-Inflammatory Mediators Axis in IgG Immune Complex-Induced Acute Lung Injury.Frontiers in immunology · 2021Article
- Suppressors of cytokine signaling 3 is essential for FcγR-mediated inflammatory response via enhancing CCAAT/enhancer-binding protein δ transcriptional activity in macrophages.Experimental cell research · 2015Article
- Protective Role of Rho Guanosine Diphosphate Dissociation Inhibitor, Ly-GDI, in Pulmonary Alveolitis.PloS one · 2015Article
- Role of p38 MAPK and STAT3 in lipopolysaccharide-stimulated mouse alveolar macrophages.Experimental and therapeutic medicine · 2014Article
- Protective actions of aspirin-triggered (17R) resolvin D1 and its analogue, 17R-hydroxy-19-para-fluorophenoxy-resolvin D1 methyl ester, in C5a-dependent IgG immune complex-induced inflammation and lung injury.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Persistence of pulmonary tertiary lymphoid tissues and anti-nuclear antibodies following cessation of cigarette smoke exposure.Respiratory research · 2014Article
- Excessive mechanical stress increases HMGB1 expression in human lung microvascular endothelial cells via STAT3.Microvascular research · 2014Article
- A large scale gene-centric association study of lung function in newly-hired female cotton textile workers with endotoxin exposure.PloS one · 2013Article
- Critical role for CCAAT/enhancer-binding protein β in immune complex-induced acute lung injury.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Molecular mechanisms of inflammation and tissue injury after major trauma--is complement the "bad guy"?Journal of biomedical science · 2011Review
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Authors and funding
7 authors at 7 institutions in 2 countries.
Funding
Abstract
Growing evidence suggests that transcription factor signal transducer and activator of transcription (Stat) 3 may play an important regulatory role during inflammation. However, the function of Stat3 in acute lung injury (ALI) is largely unknown. In the current study, by using an adenoviral vector expressing a dominant-negative Stat3 isoform (Ad-Stat3-EVA), we determined the role of Stat3 in IgG immune complex (IC)-induced inflammatory responses and injury in the lung from C57BL/6J mice. We show that IgG IC-induced DNA binding activity of Stat3 in the lung was significantly inhibited by Stat3-EVA. We demonstrate that both lung vascular permeability (albumin leak) and lung myeloperoxidase accumulation in the Ad-Stat-EVA treated mice were substantially reduced when compared with values in mice receiving control virus (Ad-GFP) during the injury. Furthermore, intratracheal administration of Ad-Stat3-EVA caused significant decreases in the contents of neutrophils, inflammatory cytokines (TNF-α and IL-6), chemokines [keratinocyte cell-derived chemokine, macrophage inflammatory protein (MIP)-1α, and MIP-1β], and complement component C5a in bronchoalveolar lavage fluids. Using Stat3-specific small interfering RNA, we show that knocking down Stat3 expression in alveolar macrophages (MH-S cells) significantly reduced the production of proinflammatory mediators on IgG IC stimulation. These data suggest that Stat3 plays an essential role in the pathogenesis of IgG IC-induced ALI by mediating the acute inflammatory responses in the lung and alveolar macrophages.
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Registered trials
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