How DNA may affect your seasonal allergies
A sniffle here, a clearing of the throat over there. And a persistent itching of the eyes. Sound familiar? With the winter weather (slowly) receding, allergy season is upon us, and you may start to see an increase in the number of people sneezing or coughing—more spring flowers bring more spring allergens. It’s only natural to wonder why some people get to go outdoors, blissfully unaffected, while others experience a host of unpleasant symptoms. The keen observer might even note that allergies seem to run in families. So, are allergies a result of genetics?
In academic literature, you’re likely to see seasonal allergies called by the more technical name allergic rhinitis. This term specifically describes symptoms involving the nose, but is the main focus of many allergy related studies (alongside terms like conjunctivitis, meaning eye inflammation). It’s difficult to nail down just how many people experience allergic rhinitis, but estimates range between 9 and 40% of some populations with most studies landing somewhere between 15 and 30%1-4. Needless to say, that’s a lot of people!
Researchers interested in the genetics of allergic reactions have studied the prevalence of allergy symptoms in families with twins1. These studies have shown us that many factors can influence the development of allergic rhinitis including a person’s environment—and their DNA. Ongoing studies are trying to identify what parts of the DNA are responsible for allergy development. While no clear answer has arisen, many signs point to segments of DNA that influences the immune system1,2.
Breaking down the name here can be helpful as we talk about what allergies actually are. The beginning of the word, rhin, means “nose.” The ending, -itis, indicates inflammation. Putting them together, the term rhinitis means an inflammation of the nose. More specifically, it refers to irritation or inflammation of the inner mucosal barrier within the nose. As unpleasant as rhinitis is, it actually serves an important function. Like your throat, your nose is a place where foreign pathogens can enter the body. Harmful chemicals, bacteria, viruses—they can all be inhaled through the nose which has provoked the evolution of defense systems. Your nose, throat, lungs, and other tissues are equipped with numerous layers of defensive material, including a layer of mucus. The mucus is sticky and full of proteins that can recognize (and in some cases destroy) foreign objects. If your body detects a potentially harmful substance tangled in the mucus, it simply expels it in what we commonly call a sneeze5.
But there are more elaborate defense mechanisms in place that can go awry and contribute to our allergies. Sitting just beyond the mucosal layer in the nose are a series of specialized cells. Some of them are lined with proteins whose job it is to recognize foreign molecules that make it past the mucus layer (like parts of bacteria or viruses). Once triggered by an invader, these defense proteins kick off a cascade of signals that result in numerous cellular changes. Like a fire alarm going off, cells surrounding the area are provoked into action where they release chemicals such as histamines, prostaglandins, and leukotrienes. These chemicals promote fluid production, sneezing, and activation of various types of immune cells. Some immune cells are primed and ready to engulf any foreign invader, while others may be prompted to produce antibodies that will specifically identify the foreign invader. This multi-tiered response helps keep us safe from potentially dangerous infections, but sometimes it can be tricked1-3.
People who have experienced allergies understand that sometimes non-bacterial invaders can provoke rhinitis. Common allergens include mites, pollens, and molds3. Individuals with allergic rhinitis have an immune system that recognizes some (or all) of these as potentially harmful foreign pathogens and responds accordingly. It’s not clear why the body is tricked like this or what role the DNA has in this deception, but numerous variants in the DNA have been identified which hold promise. Many of these variants occur in genes that are associated with the immune system1,2. For instance, there have been several variants identified in genes known as Toll Like Receptor genes2. These genes produce the proteins that identify invaders that make it past the mucus. Other variants affect chemicals that are released by immune cells1.
Variants in these and other genes have been correlated with allergic rhinitis, but none of them have been definitively linked with the condition yet. Studies like those summarized here indicate that allergic rhinitis is a complex condition that likely involves numerous genes (also known as a polygenic trait). It’s also worth noting that the effect size of these variants is also very small—meaning inheriting these variants may only have a very small influence on whether you develop allergies or not1. Still, these studies are promising and provide plenty of data to direct future studies.
We’re still in the early stages of understanding how a person’s genetics and environment interact to promote allergic rhinitis. With many exciting leads, we’ll likely see more findings in the coming years—and if that someday leads to less sneezing and fewer itchy eyes, all the better.
2Gao, Zhiwei, Donna C Rennie, and Ambikaipakan Senthilselvan. “Allergic Rhinitis and Genetic Components: Focus on Toll-like Receptors (TLRs) Gene Polymorphism.” The Application of Clinical Genetics 3 (2010): 109–120. PMC. Web. 28 Mar. 2018.
3Wheatley, Lisa M., and Alkis Togias. “Allergic Rhinitis.” The New England journal of medicine 372.5 (2015): 456–463. PMC. Web. 28 Mar. 2018.
4Melvin, Thuy-Anh N., and Murugappan Ramanathan. “Role of Innate Immunity in the Pathogenesis of Allergic Rhinitis.” Current Opinion in Otolaryngology & Head and Neck Surgery, vol. 20, no. 3, 2012, pp. 194–198., doi:10.1097/moo.0b013e3283533632.
5Songu, Murat, and Cemal Cingi. “Sneeze reflex: facts and fiction.” Therapeutic Advances in Respiratory Disease, vol. 3, no. 3, 2009, pp. 131–141., doi:10.1177/1753465809340571. Web. 28 Mar. 2018.