
A new study that examined the molecular drivers of severe asthma and rhinovirus-induced asthma exacerbation (typically associated with the common cold) looked at the therapeutic impact of blocking interactions between histamine-releasing factor (HRF) and immunoglobulin E antibodies (IgE).
The study was conducted by the Center for Autoimmunity and Inflammation at California’s La Jolla Institute for Immunology (LJI). Researcher and LJI professor Toshiaki Kawakami, MD, PhD, said the seriousness of asthma warranted such a study, as an estimated 10 individuals die each day from asthma and the disease results in 439,000 hospitalizations and 1.3 million emergency room visits annually.
“Asthma is one of the most important allergic diseases to study,” Dr. Kawakami said. Many people who have severe asthma and rhinovirus-induced asthma exacerbation aren’t responsive to current asthma treatments. Inhibiting HRF and IgE interactions might one day deliver relief to this group of patients.
HRF molecules, which is partially made up of lung epithelial cells and immune cells called macrophages, kick into action when encountering allergens. This increases HRF production, which often binds to special antibodies like IgE. In mouse models, the interaction between the two caused harmful inflammation.
According to Dr. Kawakami, researchers examined HRF levels and IgE interactions in healthy adult controls, adults infected with rhinovirus, adults with moderate and severe asthma, adults with mild-to-moderate asthma, asthmatic children with non-viral asthma exacerbation and asthmatic children with rhinovirus-induced asthma exacerbation. Not all asthma “endotypes” respond to the same therapy, Dr. Kawakami said.
The study found that the HRF and IgE interactions were stronger in patients with severe asthma and patients with rhinovirus-induced asthma exacerbation. Additionally, researchers confirmed the importance of HRF and IgE
As a result of the study, Dr. Kawakami and his team hope to test two potential asthma therapies — one that harnesses a molecule developed in his lab. Known as HRF-2CA, this molecular therapy would inhibit asthma and severe food allergy symptoms as it does in mice. The other therapy, known as SPF7-1, acts as an HRF decoy, binding with IgE and freeing the real HRF.
“The best way forward would be to carry out clinical trials to study these two therapeutic options,” Dr. Kawakami said.