Guillermina Juliana Baay-Guzman1, Sara Huerta-Yepez1, Mario I Vega2, Diana Aguilar-Leon3, Monica Campillos4, Jonathon Blake4, Vladimir Benes4, Rogelio Hernandez-Pando3, Luis M Teran5. 1. Unidad de Investigacion en Enfermedades Oncologicas, Hospital Infantil de Mexico, Federico Gomez, Mexico City, Mexico. 2. Unidad de Investigación Medica en Oncologia, CMN sXXI IMSS, Mexico City, Mexico. 3. Experimental Pathology Section, Department of Pathology, National Institute of Medical Sciences and Nutrition "Salvador Zubirán," Mexico City, Mexico. 4. European Molecular Biology Laboratory (EMBL), Heidelberg, Germany. 5. Department of Allergy and Clinical Immunology, Instituto Nacional de Enfermedades Respiratorias, Mexico City, Mexico. Electronic address: lmteran@iner.gob.mx.
Abstract
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.
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.
Authors: Stephanie Bond; Renaud Léguillette; Eric A Richard; Laurent Couetil; Jean-Pierre Lavoie; James G Martin; R Scott Pirie Journal: J Vet Intern Med Date: 2018-10-07 Impact factor: 3.333
Authors: S Björkander; C Carvalho-Queiroz; J Hallberg; J-O Persson; M A Johansson; B Nussbaum; M C Jenmalm; C Nilsson; E Sverremark-Ekström Journal: Clin Exp Immunol Date: 2020-08-05 Impact factor: 4.330