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*
Department of Pathology and
Division of Pulmonary and Critical Care, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI 48109;
Department of Pathology, Veteran Affairs Medical Center, Ann Arbor, MI 48105; and
§
Department of Medicine, Children’s Hospital and Harvard Medical School, Boston, MA 02115
Asthmatic-like reactions characterized by elevated IgE, Th2
cytokines, C-C chemokines, eosinophilic inflammation, and persistent
airway hyperresponsiveness follow pulmonary exposure to the spores or
conidia from Aspergillus fumigatus fungus in sensitized
individuals. In addition to these features, subepithelial fibrosis and
goblet cell hyperplasia characterizes fungal-induced allergic airway
disease in mice. Because lung concentrations of macrophage inflammatory
protein-1
and RANTES were significantly elevated after A.
fumigatus-sensitized mice received an intrapulmonary challenge
with A. fumigatus spores or conidia, the present study
addressed the role of their receptor, C-C chemokine receptor 1 (CCR1),
in this model. A. fumigatus-sensitized CCR1 wild-type
(+/+) and CCR1 knockout (-/-) mice exhibited similar increases in
serum IgE and polymorphonuclear leukocyte numbers in the
bronchoalveolar lavage. Airway hyperresponsiveness was prominent in
both groups of mice at 30 days after an intrapulmonary challenge with
A. fumigatus spores or conidia. However, whole lung
levels of IFN-
were significantly higher whereas IL-4, IL-13, and
Th2-inducible chemokines such as C10, eotaxin, and macrophage-derived
chemokine were significantly lower in whole lung samples from
CCR1-/- mice compared with CCR1+/+ mice at 30
days after the conidia challenge. Likewise, significantly fewer goblet
cells and less subepithelial fibrosis were observed around large
airways in CCR1-/- mice at the same time after the
conidia challenge. Thus, these findings demonstrate that CCR1 is a
major contributor to the airway remodeling responses that arise from
A. fumigatus-induced allergic airway
disease.
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