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Early Immunological Response to German Cockroach Frass Exposure Induces a Th2/Th17 EnvironmentPage K.a, c · Zhou P.a · Ledford J.R.a · Day S.B.a · Lutfi R.a · Dienger K.b · Lewkowich I.P.b
Divisions of aCritical Care Medicine and bImmunobiology, Cincinnati Children’s Hospital Medical Center and Cincinnati Children’s Research Foundation, and cDepartment of Pediatrics, University of Cincinnati, Cincinnati, Ohio, USA Corresponding Author
Dr. Kristen Page
Division of Critical Care Medicine
Cincinnati Children’s Hospital Medical Center
3333 Burnet Avenue, ML 7006, Cincinnati, OH 45229 (USA)
Tel. +1 513 636 3079, Fax +1 513 636 4267, E-Mail email@example.com
Cockroach exposure is a major risk factor for the development of asthma; however, the early immune events induced by cockroach leading to the Th2 response are not fully understood. Exposure of naïve mice to German cockroach (GC) feces (frass) was sufficient to induce dendritic cell (DC) recruiting and activating chemokines C-C motif ligand 20, granulocyte macrophage colony-stimulating factor, granulocyte colony-stimulating factor and macrophage inflammatory protein-1α into the airways. This corresponded with an increase in myeloid DCs (mDCs) in the airways as well as increased expression of CD80 and CD86 on the mDCs. Plasmacytoid DCs in the lung were unchanged. Levels of IL-5, IL-17A and IL-6 cytokines in whole lung cultures were significantly increased 18 h following GC frass exposure demonstrating the early development of a mixed Th2/Th17 response. In addition, GC frass stimulated the production of IL-23, IL-6 and IL-12p70 from bone marrow-derived mDCs. Adoptive transfer of GC frass-pulsed mDCs induced airway reactivity, airway inflammation as well as eosinophilia and induced a strong Th2/Th17 response in the lung. MyD88-deficient bone marrow-derived mDCs did not respond to GC frass treatment, suggesting a functional Toll-like receptor pathway was important to induce the Th2/Th17 response. Together, our data show that GC frass activated the innate immune response to augment DC recruitment and activation of mDCs which promoted robust T cell-skewing cytokines and ultimately drive the development of airway inflammation.
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