Mice that express a particular protein in their lungs develop an asthma-like disease very similar to human asthma and other allergic inflammatory diseases. This new finding reported in the September issue of Nature Immunology opens up new ways of studying how disabling lung inflammation may be prevented.
Asthma is the most common serious chronic disease of childhood, affecting nearly five million children in the United States alone. The hallmarks of human asthma and allergy include increased numbers of immune cells in lung tissue. These cells are the key players responsible for secreting inflammatory factors that lead to the clinical symptoms associated with asthma. Many of the processes that subsequently lead to severe lung inflammation are known and most current treatments for allergy and asthma are aimed at blocking them. Unfortunately, most of these treatments only alleviate symptoms rather than prevent their underlying causes.
Steven Ziegler and colleagues provide clues that may allow treatments to prevent lung inflammation from occurring in the first place. The team studied a protein already known to be associated with inflammation, thymic stromal lymphopoetin (TSLP), to see if it was also responsible for symptoms of severe lung inflammation in mice. Mice that produced TSLP specifically in lung cells showed greatly increased disease that had most of the hallmarks of human asthma and other allergic inflammatory diseases. Zeigler and colleagues also evaluated mice that were deficient in TSLP, and these mice showed few signs of lung inflammation and failed to develop asthma-like disease.
Importantly, this work shows that a single protein is a key factor in the appearance of lung inflammatory disease, which may open up new avenues of research into treatments that prevent lung inflammation before the onset of debilitating symptoms.
Steven Ziegler (Benaroya Research Institute, Seattle, WA, USA)
For abstract, click here.
(C) Nature Immunology press release.
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