Asthma often begins early in life and is attributed to more
than just genetic factors, because the prevalence continues to rise. Epidemiological
studies have indicated roles for prenatal and early childhood exposures,
including exposure to diesel exhaust, however, little is known about the
mechanisms involved. To elucidate this, Manners et al developed a mouse model
of asthma susceptibility through prenatal exposure to diesel exhaust (J Allergy Clin Immunol 2014; 134(1): 63-72).
In this
model, pregnant mice were repeatedly exposed to diesel exhaust particles
(DEPs). Offspring were immunized and challenged with ovalbumin (OVA) or exposed to PBS (control) then examined
for features of asthma. Compared
to controls, offspring that were exposed to DEP were hypersensitive to OVA,
indicated by airway hyperresponsiveness, elevated serum levels of OVA-specific
IgE, and elevated levels of pulmonary and systemic T-helper type 2 (Th2) and
Th17 cytokines. The authors determined that natural killer (NK) cells were the
primary source of cytokine production and airway inflammation was diminished by
antibody-mediated depletion of NK cells. Furthermore, asthma susceptibility was
associated with increased transcription of genes known to be specifically
regulated by the aryl hydrocarbon receptor (AhR) and oxidative stress.
These results coincide with previous data that suggests NK
cells initiate allergic inflammation. AhR is expressed in NK cells which may
provide a link between maternal exposure to diesel exhaust and asthma in
offspring. Taken together, this data provides mechanistic insight into the
process of prenatally-induced asthma
susceptibility.
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