NDLI: Carbonic anhydrase IV is expressed on IL-5-activated murine eosinophils.

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Carbonic anhydrase IV is expressed on IL-5-activated murine eosinophils.

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Carbonic anhydrase IV is expressed on IL-5-activated murine eosinophils.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Mingler, Melissa K. Wahl, Benjamin Pabst, Oliver Wen, Ting Khorki, M. Eyad Rothenberg, Marc E. Zimmermann, Nives
Description	Author Affiliation: Wen T ( Division of Allergy and Immunology, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, OH 45229); Mingler MK ( Division of Allergy and Immunology, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, OH 45229); Wahl B ( Institute of Immunology, Hannover Medical School, 30625 Hannover, Germany.); Khorki ME ( Division of Allergy and Immunology, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, OH 45229); Pabst O ( Institute of Immunology, Hannover Medical School, 30625 Hannover, Germany.); Zimmermann N ( Division of Allergy and Immunology, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, OH 45229); Rothenberg ME ( Division of Allergy and Immunology, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, OH 45229)
Abstract	Eosinophilia and its cellular activation are hallmark features of asthma, as well as other allergic/Th2 disorders, yet there are few, if any, reliable surface markers of eosinophil activation. We have used a FACS-based genome-wide screening system to identify transcriptional alterations in murine lung eosinophils recruited and activated by pulmonary allergen exposure. Using a relatively stringent screen with false-positive correction, we identified 82 candidate genes that could serve as eosinophil activation markers and/or pathogenic effector markers in asthma. Carbonic anhydrase IV (Car4) was a top dysregulated gene with 36-fold induction in allergen-elicited pulmonary eosinophils, which was validated by quantitative PCR, immunohistochemistry, and flow cytometry. Eosinophil CAR4 expression was kinetically regulated by IL-5, but not IL-13. IL-5 was both necessary and sufficient for induction of eosinophil CAR4. Although CAR4-deficient mice did not have a defect in eosinophil recruitment to the lung, nor a change in eosinophil pH-buffering capacity, allergen-challenged chimeric mice that contained Car4(-/-) hematopoietic cells aberrantly expressed a series of genes enriched in biological processes involved in epithelial differentiation, keratinization, and anion exchange. In conclusion, we have determined that eosinophils express CAR4 following IL-5 or allergen exposure, and that CAR4 is involved in regulating the lung transcriptome associated with allergic airway inflammation; therefore, CAR4 has potential value for diagnosing and monitoring eosinophilic responses.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1302846
Journal	The Journal of Immunology
Issue Number	12
Volume Number	192
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2014-06-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Asthma Immunology Carbonic Anhydrase Iv Eosinophils Interleukin-5 Allergens Genetics Animals Diagnosis Metabolism Pathology Biosynthesis Cell Differentiation Enzyme Induction Hematopoietic Stem Cells Interleukin-13 Lung Mice Mice, Knockout Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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