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Updated: May 10, 2026

An IL-8 Transiently Transgenized Mouse Model for the In Vivo Long-term Monitoring of Inflammatory Responses
Published on: July 7, 2017
Interleukin 8 and acute lung injury
Timothy Craig Allen1, Anna Kurdowska
1From the Departments of Pathology (Dr Allen) and Biochemistry (Dr Kurdowska), University of Texas Health Science Center at Tyler. Dr Allen is now located at the University of Texas Medical Branch at Galveston, Texas.
Abstract:
Acute lung injury is a complex clinical syndrome involving acute inflammation, microvascular damage, and increased pulmonary vascular and epithelial permeability, frequently resulting in acute respiratory failure culminating in often-fatal acute respiratory distress syndrome. Interleukin 8 (IL-8), a potent neutrophil attractant and activator, plays a significant role in acute lung injury via the formation of anti-IL-8 autoantibody:IL-8 complexes and those complexes' interaction with FcγRIIa receptors, leading to the development of acute lung injury by, among other possible mechanisms, effecting neutrophil apoptosis. These complexes may also interact with lung endothelial cells in patients with acute respiratory distress syndrome. Continuing research of the role of neutrophils, IL-8, anti-IL-8 autoantibody:IL-8 complexes, and FcγRIIa receptors may ultimately provide molecular therapies that could lower acute respiratory distress syndrome mortality, as well as reduce or even prevent the development of acute lung injury altogether.
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