Apr 27, 2017 04:18 AM EDT
A new research in mice by the University of California San Francisco has discovered that an ancient and specialized enzyme is capable of destroying of the compound from bugs and molds that could affect our lungs. This means that people who lack with this enzyme are more vulnerable to diseases caused by this compound.
The compound, which is called chitin (pronounced as /kai-tin/), could be found on beetle's and crab's shell that makes it strong and sturdy. These insects and crustaceans produce billions of chitin every year and without the enzyme that was secreted by people, it would accumulate in the airways and cause inflammatory lung diseases.
This enzyme that specializes in breaking down and disposing of this chitin, called chitinases, has evolved in history and was mostly shared by most living things like single-celled bacteria, fungi, and humans. Until now, the function of this enzyme was a mystery to science.
In the study published online in Cell called it has shown that the mice that lacked in enzymes designed to destroy chitins accumulated chitin in their lungs and developed severe inflammatory lung diseases. The research team also found out that they could restore the function of the lungs of these ailing mice by replacing the chitinase enzymes with a finding that could have implications for understanding and treating age-related lung diseases among humans.
"We were very excited to see that improving chitinase activity quickly cleared up the signs of chronic inflammatory lung disease in these mice," Dr. Richard Locksley, the senior author of the study has said. He added that this is the first demonstration that chitinases play a key role in preserving lung function in vertebrates, according to the article published by University of California San Francisco official website.
This study was funded by the National Institutes of Health, the Howard Hughes Medical Institute, the Nina Ireland Program for Lung Health, and the Sandler Asthma Basic Research Center at UCSF. Other authors of this paper were Hong-Erh Liang, Ram P. Naikawadi, Dr. Prescott G. Woodruff, Dr. Paul J. Wolters, and Dr. David J. Erle.
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