Transient expression of IL-1beta induces acute lung injury and chronic repair leading to pulmonary fibrosis.
By M. Kolb, P. Margetts, D. Anthony, F. Pitossi, J. Gauldie. Journal of Clinical Investigation, 2001
784 citations recorded by the source corpus.
Subfields: Public Health, Environmental and Occupational Health, Pulmonary and Respiratory Medicine
View Paper: https://www.semanticscholar.org/paper/f7d131fba1168962f71ec533f377b59decbd492d
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Pulmonary and Respiratory Medicine
Citations in the corpus
- Integrating mechanisms of pulmonary fibrosis (2011, background): “Like TNF, IL-1 can induce acute lung injury and may contribute to the progression of pulmonary fibrosis (Kolb et al., 2001).”
- Regulation of PDGF and its receptors in fibrotic diseases. (2004, background): “[29] Kolb M, Margetts PJ, Anthony DC, Pitossi F, Gauldie J.”
- IL-17, Produced by Lymphocytes and Neutrophils, Is Necessary for Lipopolysaccharide-Induced Airway Neutrophilia: IL-15 as a Possible Trigger (2003, background): “(30, 31) or direct application into the lung (27, 32) resulted in a”
- NLRP3 inflammasome activation results in hepatocyte pyroptosis, liver inflammation and fibrosis (2014, background): “Moreover, transient expression of IL-1b in airway epithelial cells promoted a significant increase in TGF-b and associated deposition of collagen in the lung.(36) Furthermore, HCSs, the myofibroblasts of the liver, can be activated either by IL-1b or IL-18 to induce collagen deposition.”
- Murine models of pulmonary fibrosis. (2008, background): “In mice, the fibrotic response is associated with limited and transient inflammation and overexpression of the anti-inflammatory cytokine, IL-10.”