In a new study entitled “Structure-Function Analysis of CCL28 in the Development of Post-viral Asthma,” researchers identified that a chemokine protein structure, CCL28, is a key factor in the development of asthma pathology. The study was published in the Journal of Biological Chemistry.
Asthma is a chronic inflammatory disease of the air passages characterized by airflow obstruction and with common symptoms of wheezing, coughing and shortness of breath. Currently, there is no cure for asthma and affects approximately 25 million people, including young children, in the United States alone, according to the Centers for Disease Control and Prevention.
In this study, a research team at the Medical College of Wisconsin tackled previous reports that identified a human signaling protein secreted by cells (chemokine) – CCL28 – to be highly expressed in the airways of asthma patients, suggesting that CCL28 is a crucial player in acute development of post-viral asthma, i.e., when viruses are the underlying cause of asthma symptoms. In the study, the authors show that even in the absence of viral infections, CCL28 can promote asthma pathology, and they identified that the cause was related to the CCL28 protein folding status — the process by which proteins acquire a defined structure that is key for its functional activity in cells. Specifically, the team discovered that CCL28 when folded in its native form promotes the attraction of mouse subset of T cells (CD4+ T-cell), which are recognized as important mediators of inflammation and in vivo hyper reactivity in the airways.
The researchers’ findings suggest that new therapeutics to prevent the development of post-viral asthma may be achieved by targeting the characteristics of the CCL28 structure.
Brian F. Volkman, PhD, professor of biochemistry and study lead author, together with Mitchell H. Grayson, MD, associate professor of allergy and immunology, commented in a press release, “We found that even in the absence of a viral infection, CCL28 can play a role in the induction of asthma pathology — when the protein is natively folded. If unfolded, it does not. We propose that by exploiting the unique structural features of CCL28, potent and specific CCL28 inhibitors may be developed. This work is the first step in generating a novel type of asthma therapy that may have the power to prevent development of post-viral asthma in young children.”
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