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From the Department of Pathology,* University ofMichigan Medical School, Ann Arbor, Michigan; the Rega Institute forMedical Research, Leuven, Belgium; andAnorMED, Incorporated, Langley, BritishColumbia, Canada
The role of specific chemokine receptors during allergic asthmatic
responses has been relatively undefined. A number of receptors are
preferentially expressed on Th2 cells, including CCR4,
CCR8, and CxCR4. In the present study, we have examined
the role of CxCR4 in the development of cockroach allergen-induced
inflammation and airway hyperreactivity in a mouse model of asthma.
Using a specific inhibitor of CxCR4, AMD3100, our
results indicate that blocking this receptor has a significant effect
in down-regulating the inflammation and pathophysiology of the
allergen-induced response. Treatment of allergic mice with AMD3100
significantly reduced airway hyperreactivity, peribronchial
eosinophilia, and the overall inflammatory responses. In
addition, there was a shift in the cytokine profile that was
observed in the AMD3100-treated animals. Specifically, there
was a significant reduction in interleukin-4 and interleukin-5 levels
and a significant increase in interleukin-12 and interferon-
levels
within the lungs of treated allergic mice. Furthermore, there
was a significant alteration in the local chemokine production of CCL22
(MDC) and CCL17 (TARC), two chemokines previously shown to be
important in Th2-type allergen responses. Overall, specifically
blocking CxCR4 using AMD3100 reduced a number of pathological
parameters related to asthmatic-type inflammation.
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