Chuck Bednar for redOrbit.com – @BednarChuck
New research from the Medical College of Wisconsin (MCW) and the Children’s Hospital of Wisconsin Research Institute has linked a specific type of protein to the development of viral-induced asthma – a discovery that could help treat the condition in young children.
In the study, MCW biochemistry professor Dr. Brian F. Volkman, Dr. Mitchell H. Grayson of the CHW Research Institute and their colleagues report that CCL28, a human chemokine that is expressed by columnar epithelial cells and which has been shown to attract various types of immune cells, is associated with the pathogenesis of acute post-viral asthma.
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“Elevated levels of CCL28 have been found in the airways of individuals with asthma, and previous studies have indicated that CCL28 plays a vital role in the acute development of post-viral asthma,” they wrote in a recent edition of the Journal of Biological Chemistry. “Our study builds on this, demonstrating that CCL28 is also important in the chronic post-viral asthma phenotype… [and] is both necessary and sufficient for induction of asthma pathology.”
Looking for preventative measures
Asthma, a chronic condition of the respiratory system affecting more than 300 million people worldwide, is the primary cause of illness-related school absences in children, the study authors explained. It also accounts for more than 1.8 million emergency room visits annually, and since there is no cure, the focus is on treating symptoms and preventing severe attacks.
Dr. Grayson and Dr. Volkman had previously found evidence linking CCL28 to the development of chronic asthma, but this new study is the first to analyze the structural features of the human chemokine and its impact on the development of the disease. They found that its structure is vital to its role in pathogenesis, and that inhibiting the protein could help prevent post-viral asthma.
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“Understanding the molecular mechanisms by which asthma develops and establishes itself as a chronic disease is key to elucidating alternative and potentially curative therapies,” explained Dr. Grayson, who is also the director of Fight Asthma Milwaukee (FAM) Allies and a member of the board of directors of the national Asthma and Allergy Foundation of America.
“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,” added Dr. Volkman, calling it “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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By exploiting the unique structural features of the protein, the study authors said, powerful and specific CCL28 inhibitors could be developed. Because of the “intimate relationship” between the chemokine and asthma pathology, CCL28 could well be “a novel target for the development of alternative asthma theraputics,” they added.
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