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The pathomechanism of this phenomenon has not been fully understood. Here, we evaluated the immunological mechanisms and the role of the prostaglandin D\n                    <jats:sub>2<\/jats:sub>\n                    \/ Chemoattractant Receptor\u2010Homologous Molecule Expressed on Th2 Cells (CRTH2) pathway in the development of\n                    <jats:italic>Aspergillus<\/jats:italic>\n                    \u2010associated asthma exacerbation. We studied the effects of\n                    <jats:italic>\n                      <jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>\n                      .\u00a0fumigatus\n                    <\/jats:italic>\n                    on airway inflammation and bronchial hyper\u2010responsiveness in a rat model of chronic asthma. Inhalation delivery of\n                    <jats:italic>\n                      <jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>\n                      .\u00a0fumigatus\n                    <\/jats:italic>\n                    conidia increased the airway eosinophilia and bronchial hyper\u2010responsiveness in ovalbumin\u2010sensitized, challenged rats. These changes were associated with prostaglandin D\n                    <jats:sub>2<\/jats:sub>\n                    synthesis and\n                    <jats:styled-content style=\"fixed-case\">CRTH<\/jats:styled-content>\n                    2 expression in the lungs. Direct inflammation occurred in ovalbumin\u2010sensitized, challenged animals, whereas pre\u2010treatment with an antagonist against\n                    <jats:styled-content style=\"fixed-case\">CRTH<\/jats:styled-content>\n                    2 nearly completely eliminated the\n                    <jats:italic>\n                      <jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>\n                      .\u00a0fumigatus\n                    <\/jats:italic>\n                    \u2010induced worsening of airway eosinophilia and bronchial hyper\u2010responsiveness. Our data demonstrate that production of prostaglandin D\n                    <jats:sub>2<\/jats:sub>\n                    followed by eosinophil recruitment into the airways via a\n                    <jats:styled-content style=\"fixed-case\">CRTH<\/jats:styled-content>\n                    2 receptor are the major pathogenic factors responsible for the\n                    <jats:italic>\n                      <jats:styled-content style=\"fixed-case\">A<\/jats:styled-content>\n                      .\u00a0fumigatus\n                    <\/jats:italic>\n                    \u2010induced enhancement of airway inflammation and responsiveness.\n                  <\/jats:p>","DOI":"10.1111\/imm.12234","type":"journal-article","created":{"date-parts":[[2013,12,16]],"date-time":"2013-12-16T04:56:56Z","timestamp":1387169816000},"page":"78-88","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":15,"title":["Role of prostaglandin D\n        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