Dr. Michelle Gill, assistant
professor of pediatrics and internal medicine at UT Southwestern
and lead author of the study appearing online and in the June
edition of the Journal of...
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DALLAS – June 1, 2024 – New research from UT
Southwestern Medical Center suggests that allergic reactions to pet
dander, dust mites and mold may prevent people with allergic asthma
from generating a healthy immune response to respiratory viruses
such as influenza.
"Our findings imply that the better your asthma is controlled,
the more likely you are to have an appropriate response to a
virus," said Dr. Michelle Gill, assistant professor of pediatrics
and internal medicine at UT Southwestern and lead author of the
study appearing online and in the June edition of the Journal of
Immunology. "When individuals with asthma come in contact with
an allergic trigger and a respiratory virus, the allergen may
actually interfere with the immune response to the virus. This
interruption in the antiviral response may contribute to
exacerbations of asthma that are commonly associated with
respiratory viral infections."
More than half of the 20 million people diagnosed with asthma in
the U.S., including 2.5 million children, have been diagnosed with
allergic asthma.
Fifty-six people ranging in age from 3 to 35 participated in the
study. Twenty-six of the participants suffered from allergic
asthma; the remaining 30 made up the control group. Most of the
participants were African-American, and the mean age was 15 years
in both the asthma and control groups. In addition, those in the
asthma group had been diagnosed by a physician and had a positive
skin test to at least one indoor allergen.
Researchers first isolated immune cells called dendritic cells
from study participants. These cells are found in blood and tissues
that are in contact with the environment, such as skin and the
linings of the nose and lungs. When they encounter respiratory
viruses such as flu, dendritic cells normally produce proteins that
help the body mobilize the immune system and overcome the viral
infection. When the dendritic cells first encounter an allergic
stimulus, however, they are significantly impaired in their ability
to produce such antiviral proteins.
When investigators exposed the dendritic cells from the study
participants with allergic asthma to influenza, they found that the
cells were unable to produce interferon, an immune system protein
that plays a key role in fighting off repeated infections of the
same virus. Interferon is what makes a person feel run down and
tired when fighting viral infections.
The researchers speculate that the immune-suppressing effect of
the allergic stimulation of dendritic cells might be related to the
high levels of a molecule called IgE normally found in people with
allergic asthma. Among the subjects participating in this study,
elevated IgE levels were associated with impaired capacity of
dendritic cells to produce interferon when exposed to flu.
Dr. Gill said these findings suggest that when the cold/flu and
allergy seasons collide, the immune response in individuals with
allergic asthma may worsen their disease.
"These findings imply that allergic triggers associated with
exposure to indoor allergens like pet dander and dust mites can
potentially render cells deficient in responding to a virus," Dr.
Gill said. "It may – although this remains to be proven
– also explain why asthmatics who are sensitive to indoor
allergens often experience asthma exacerbations when they acquire
respiratory viral infections."
The findings from this study prompted an upcoming mechanistic
study of dendritic cells as part of the Inner City Asthma
Consortium (ICAC), which receives funding through the National
Institute of Allergy and Infectious Diseases. The dendritic cell
component of the ICAC study will investigate whether a treatment to
lower IgE in allergic asthma patients will improve dendritic cells'
response to allergens and respiratory viruses. UT Southwestern is
among 10 institutions involved in the ICAC, which is administered
by the University of Wisconsin-Madison.
SOURCE