The Four-Letter-C-Word: Could a potential gene-based cure for asthma be on the scientific radar?

Before I start, I meet any claims including the “c-word”—cure—with extreme caution. However scientific the claims may be, however sound the rationale behind the potential curative thing may be, I do not allow myself to get too hopeful—while still having hope. I live with asthma day in and day out, and I don’t see that changing in my lifetime.

Now, with that said, there has certainly been some exciting genetics-related news out of the United Kingdom, specifically from researchers at University of Southampton. Researchers have long known that asthma seems to have a genetic component—after all, you are more likely to have asthma if someone else in your family has asthma, allergies or eczema, and often, we can see these patterns in our own families. By isolating what gene we believe causes asthma, we could theoretically develop a treatment or drug to “block” the effects of that gene on the lungs—stop it from happening completely, or, in this case, prevent asthma from worsening. For years, this has been an arduous task for asthma researchers.

This new research, led by Dr. Hans Michel Haitchi’s team, suggests that a gene known as ADAM33 (or, if you want more of a mouthful, the “a disintegrin and metalloprotease 33” gene could be the cause of asthma development. 1 By blocking this gene—stopping it dead in its tracks from affecting the lungs, or at least stopping effects that have already developed—we could stop asthma from developing or getting worse 1. It is said that ADAM33, in studies on mice, is responsible for airway inflammation, a core problem in asthma along with airway constriction, as well as airway remodelling1—a problem that usually affects people with more severe asthma, and causes a degree of irreversible airway obstruction that leads to worsened asthma symptoms and exacerbations. When mice—who are genetically similar to humans—who were positive for this gene, experience a cascade of effects via an enzyme that, in asthmatics, “loses its grip” on the cell previously (and appropriately) attached to travels to the lungs, causing increased smooth muscle development (smooth muscle wraps around the airways and is what causes our lungs to clamp up, or the airways to “tighten”, by squeezing during an asthma flare).1The enzyme alone, though, did not cause increased airway inflammation among mice—however, when these mice were exposed to dust mites, a common allergen among those of us with asthma, many mice then experienced airway inflammation and—eventually—airway remodelling.1 

From this, we learn that both the ADAM33 gene AND an allergic component to asthma, need to exist for asthma to develop. 1 However, little else is known about the ADAM33 gene beside this link to asthma, its location on chromosome 20, and that is related to snake venom—which is kind of cool, and where the “disintegrin” component; this component in snake venom is what stops blood from clotting around the site of a snake bite 2,3,. Snake-unrelated, however, it could be awhile before researchers learn what is necessary to block the gene in humans and stop asthma. The interesting—and most promising—thing though? When the gene was deactivated in mice in utero, who had experienced airway remodelling, the airway remodelling reversed  1—meaning, if this is true in humans, even if asthma is not completely reversed by deactivation of the gene, it should become significantly less severe by re-opening previously narrowed remodelled airways.  1

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