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Original Research |

Role of CXCL13 in AsthmaCXCL13 in Asthma: Novel Therapeutic Target

Guillermina Juliana Baay-Guzman, PhD; Sara Huerta-Yepez, PhD; Mario I. Vega, PhD; Diana Aguilar-Leon, PhD; Monica Campillos, PhD; Jonathon Blake, PhD; Vladimir Benes, PhD; Rogelio Hernandez-Pando, MD, PhD; Luis M. Teran, MD, PhD
Author and Funding Information

From the Unidad de Investigacion en Enfermedades Oncologicas (Drs Baay-Guzman and Huerta-Yepez), Hospital Infantil de Mexico, Federico Gomez, Mexico City, Mexico; Unidad de Investigación Medica en Oncologia (Dr Vega), CMN sXXI IMSS, Mexico City, Mexico; Experimental Pathology Section (Drs Aguilar-Leon and Hernandez-Pando), Department of Pathology, National Institute of Medical Sciences and Nutrition “Salvador Zubirán,” Mexico City, Mexico; European Molecular Biology Laboratory (EMBL) (Drs Campillos, Blake, and Benes), Heidelberg, Germany; and Department of Allergy and Clinical Immunology (Dr Teran), Instituto Nacional de Enfermedades Respiratorias, Mexico City, Mexico.

Correspondence to: Luis M. Teran, MD, PhD, Department of Allergy and Clinical Immunology, Instituto Nacional de Enfermedades Respiratorias, Calzada de Tlalpan 4502, CP 14080, DF, Mexico; e-mail: lmteran@iner.gob.mx


Funding/Support: This work was supported by CONACYT (grant 141084) and the Alexander von Humboldt Foundation.

Drs Baay-Guzman and Huerta-Yepez contributed equally to this work.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).


© 2012 American College of Chest Physicians


Chest. 2012;141(4):886-894. doi:10.1378/chest.11-0633
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Background:  B cells play an important role in allergic asthma. However, the mechanisms by which these cells are activated in the airways remain poorly understood.

Methods:  We used a mouse model of ovalbumin (OVA)-induced allergic inflammation to study CXCL13 and to investigate the concentration of this chemokine in the BAL fluid derived from asthmatic and normal control subjects.

Results:  We found that OVA-challenged mice upregulate the CXCL13/CXCR5 axis, which is associated with several changes in their airways, including recruitment of B and CD4+ cells, development of bronchial-associated lymphoid tissue, and airway inflammation. Treating sensitized mice with an anti-CXCL13 antibody reduced cell recruitment, bronchial-associated lymphoid tissue formation, and airways inflammation. Interestingly, measurements of CXCL13 using enzyme-linked immunosorbent assay showed that levels of this cytokine were significantly elevated in BAL fluid from subjects with asthma compared with control subjects (median, 162 [range, 120-296] vs 31 [range, 120-156] pg/mL; P = .005).

Conclusions:  All together, these findings suggest that CXCL13 is involved in the allergic airway inflammatory process, and targeting this chemokine may constitute a novel approach in asthma.

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