This is Dr. Youngman Oh's work. So, could liposomal IGFBP-3 be used for asthma.
02:26 EDT 30th March 2014 | BioPortfolio
Summary of "Targeting IGF-I and IGFBP-3 Signaling Pathways: A Novel Therapeutic Approach for Asthma."
"Insulin like growth factor I (IGF-I) has been recognized to play critical roles in the pathogenesis of asthma while insulin like growth factor binding protein 3 (IGFBP-3) blocks crucial physiologic manifestations of asthma. IGF-I enhances subepithelial fibrosis, airway inflammation, airway hyperresponsiveness (AHR), and airway smooth muscle hyperplasia by interacting with various inflammatory mediators and complex signaling pathways such as intercellular adhesion molecule-1 (ICAM-1), and the hypoxia inducible factor/vascular endothelial growth factor (HIF/VEGF) axis. On the other hand, IGFBP-3 decreases airway inflammation and AHR through IGFBP-3 receptor (IGFBP-3R)-mediated activation of caspases, which subsequently inhibits NF-κB signaling pathway. It also inhibits the IGF-I/HIF/VEGF axis via IGF-I-dependent and/or IGF-I-independent mechanisms. This review will summarize the role of IGF-I and IGFBP-3 in the context of allergic airway disease and discuss the therapeutic potential of various strategies targeting the IGF-I and IGFBP-3 signaling pathways for the management of asthma."
This is from earlier work in 2010. Nice to see they are still working on this.
"In asthma, when the airways become inflamed, they become hyperreactive, or overly sensitive, to "triggers," such as dust, smoke and pet dander. This leads to a chain of reactions that elicit an asthma "attack." According to the American Lung Association nearly 23 million people have asthma, of which 9 million are children.
"Anti-inflammatory corticosteroid medicines are an important part of asthma management for many people, but an estimated 20 percent of patients with asthma are resistant to existing steroid medications and there is a critical need for alternate therapies," Oh said.
Using a mouse model, Oh and his colleagues showed that IGFBP-3 production is suppressed in asthma. They measured NF-κB inflammatory activity, using molecular and cellular techniques, and found that treatment with IGFBP-3 blocked NF-κB activity.
The researchers administered IGFBP-3 to the mice by spraying a synthetic form of the protein into their opened trachea. The treatment "reduced all physiological manifestations of asthma," including airway inflammation and hyperreactivity, Oh said. His research team plans to study IGFBP-3 treatment in asthmatic canine models next."