How can dust mites trigger asthma?
A new way has been identified of how certain allergies can develop. Researchers deciphered the molecular mechanism over which house dust mites lead to allergies and asthma. This could also open up new approaches to the treatment and prevention of allergies.
A recent study involving the Johns Hopkins Bloomberg School of Public Health identified the sequence of molecular events that cause dust mites to trigger asthma and allergic rhinitis. The results were published in the English language journal "Nature Immunology".
Does misidentification lead to asthma?
Asthma is often triggered by dust mites, tree and grass pollen. Researchers believe that the escalating immune response occurs when the immune system mistakenly considers otherwise harmless allergens to be pieces of bacteria or other infectious agents. However, the molecular mechanisms underlying this misidentification have not yet been sufficiently understood.
What is SAA1?
The current study examined SAA1, an immune protein that can be found in the fluid that lines the respiratory tract and other mucosal surfaces. SAA1 belongs to the evolutionary innate immune system of mammals.
Interaction between mite molecules and SAA1
Allergy-inducing molecules from dust mites can interact with an immune protein called SAA1. The current study shows step by step how this interaction between mite molecules and SAA1 triggers an allergic-type immune response in mice.
The researchers found that exposure to dust mite proteins caused asthma-like airway sensitization in mice in the control group. In contrast, exposure to dust mite proteins had little effect in mice in which SAA1 was neutralized by antibodies or in mice whose genes were switched off for SAA1.
Allergic type immune reactions stimulated
Further research confirmed that, when present, SAA1 directly binds certain dust mite allergens, which are called fatty acid-binding proteins and have structural similarities to proteins found in some bacteria and parasites. This allergen-SAA1 interaction releases SAA1 in its active form by activating a receptor called FPR2 on the cells that line the airways.
The airway cells then produce and secrete large amounts of interleukin-33, a protein known for its ability to stimulate allergic-type immune responses.
How do allergens activate Interleukin-33?
The research group assumes that different allergens go different ways to activate interleukin-33 and the associated allergic reactions. The SAA1-FPR2 pathway appears to be a path that is followed by some house dust mite allergens.
How relevant are the results for people?
The researchers also see the results as relevant for humans and, according to their own information, found evidence of increased production of SAA1 and FPR2 in nasal cells of people with chronic sinusitis. This form of sinusitis is often associated with dust mite allergens.
New treatment strategy for asthma in prospect?
The results of the study show a possible way in which allergic and inflammatory diseases can arise. They also suggest that blocking this route could potentially act as a prevention or treatment strategy against asthma and other allergic reactions, the researchers emphasize. The research group believes that the signal interactions that occur immediately after the activation of SAA1 by the mite proteins could be good targets for future drugs.
Signal path also relevant for other diseases and allergies?
The newly described allergic SAA1-FPR2 signaling pathway could not only be relevant for asthma and hay fever, but also for atopic dermatitis (eczema) and food allergies, possibly even for chronic inflammatory diseases such as rheumatoid arthritis and atherosclerosis, the researchers add. (as)
Author and source information
This text corresponds to the requirements of the medical literature, medical guidelines and current studies and has been checked by medical doctors.
- Naina Gour, Jordan Phelan, Gerhard Hofer, Cordula Köhler, Bernhard Kratzer et al .: Serum amyloid A is a soluble pattern recognition receptor that drives type 2 immunity, in Nature Immunology (published June 22, 2020), Nature Immunology