ArticleCellular & molecular biology letters2018
Elevated IL-33 promotes expression of MMP2 and MMP9 via activating STAT3 in alveolar macrophages during LPS-induced acute lung injury.
Article in Cellular & molecular biology letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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50 citing papers in PubMed, 98 citations in OpenAlex.
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- BAG3 promotes proliferation and migration of arterial smooth muscle cells by regulating STAT3 phosphorylation in diabetic vascular remodeling.Cardiovascular diabetology · 2024Article
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- Obesity-induced downregulation of miR-192 exacerbates lipopolysaccharide-induced acute lung injury by promoting macrophage activation.Cellular & molecular biology letters · 2024Article
- Baicalin and lung diseases.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
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- TM9SF1 offers utility as an efficient predictor of clinical severity and mortality among acute respiratory distress syndrome patients.Frontiers in immunology · 2024Article
- The production, function, and clinical applications of IL-33 in type 2 inflammation-related respiratory diseases.Frontiers in immunology · 2024Review
- Progress in cytokine research for ARDS: A comprehensive review.Open medicine (Warsaw, Poland) · 2024Review
- Irf7 regulates the expression of Srg3 and ferroptosis axis aggravated sepsis-induced acute lung injury.Cellular & molecular biology letters · 2023Article
- The macrophage polarization by miRNAs and its potential role in the treatment of tumor and inflammation (Review).Oncology reports · 2023Review
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPulmonary inflammation and endothelial barrier permeability increase in acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) induced by pro-inflammatory cytokines and matrix metalloproteinases (MMPs). However, the relationship between pro-inflammatory cytokines and MMPs in ALI/ARDS remains poorly understood.
methodsA lipopolysaccharide (LPS)-induced ALI rat model was established through intratracheal instillation. The wet/dry ratios of lung tissues were measured, and bronchoalveolar lavage fluid (BALF) was collected to test protein concentrations, total cell/macrophage numbers, and pro-inflammatory cytokine levels. LPS-treated alveolar macrophages were utilized in in vitro experiments. The expression and secretion of MMPs were respectively detected using quantitative PCR, Western blotting and ELISA assays.
resultsThe levels of IL-33 and MMP2/9 in BALF increased in all the ALI rats with severe lung injury. LPS-induced IL-33 autocrine upregulated the expression of MMP2 and MMP9 through activating STAT3. Neutralizing IL-33 in culture medium with specific antibodies suppressed the expression and secretion of MMP2 and MMP9 in LPS-treated alveolar macrophages. Consistently, eliminating IL-33 decreased the levels of MMP2 and MMP9 in BALF and alleviated lung injury in ALI rats.
conclusionThe IL-33/STAT3/MMP2/9 regulatory pathway is activated in alveolar macrophages during acute lung injury, which may exacerbate the pulmonary inflammation.
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