Your browser doesn't support javascript.
loading
Factor XI deficiency enhances the pulmonary allergic response to house dust mite in mice independent of factor XII.
Stroo, Ingrid; Yang, Jack; de Boer, J Daan; Roelofs, Joris J T H; van 't Veer, Cornelis; Castellino, Francis J; Zeerleder, Sacha; van der Poll, Tom.
Afiliación
  • Stroo I; Center for Experimental and Molecular Medicine, University of Amsterdam, Amsterdam, the Netherlands; i.stroo@amc.uva.nl.
  • Yang J; Department of Immunopathology, Sanquin Research, Amsterdam, the Netherlands; and.
  • de Boer JD; Center for Experimental and Molecular Medicine, University of Amsterdam, Amsterdam, the Netherlands.
  • Roelofs JJ; Center for Experimental and Molecular Medicine, University of Amsterdam, Amsterdam, the Netherlands.
  • van 't Veer C; Department of Pathology, University of Amsterdam, Amsterdam, the Netherlands.
  • Castellino FJ; Center for Experimental and Molecular Medicine, University of Amsterdam, Amsterdam, the Netherlands.
  • Zeerleder S; W.M. Keck Center for Transgene Research, University of Notre Dame, Notre Dame, Indiana.
  • van der Poll T; Department of Immunopathology, Sanquin Research, Amsterdam, the Netherlands; and.
Am J Physiol Lung Cell Mol Physiol ; 312(2): L163-L171, 2017 Feb 01.
Article en En | MEDLINE | ID: mdl-27913422
Asthma is associated with activation of coagulation in the airways. The coagulation system can be initiated via the extrinsic tissue factor-dependent pathway or via the intrinsic pathway, in which the central player factor XI (FXI) can be either activated via active factor XII (FXIIa) or via thrombin. We aimed to determine the role of the intrinsic coagulation system and its possible route of activation in allergic lung inflammation induced by the clinically relevant human allergen house dust mite (HDM). Wild-type (WT), FXI knockout (KO), and FXII KO mice were subjected to repeated exposure to HDM via the airways, and inflammatory responses were compared. FXI KO mice showed increased influx of eosinophils into lung tissue, accompanied by elevated local levels of the main eosinophil chemoattractant eotaxin. Although gross lung pathology and airway mucus production did not differ between groups, FXI KO mice displayed an impaired endothelial/epithelial barrier function, as reflected by elevated levels of total protein and IgM in bronchoalveolar lavage fluid. FXI KO mice had a stronger systemic IgE response with an almost completely absent HDM-specific IgG1 response. The phenotype of FXII KO mice was, except for a higher HDM-specific IgG1 response, similar to that of WT mice. In conclusion, FXI attenuates part of the allergic response to repeated administration of HDM in the airways by a mechanism that is independent of activation via FXII.
Asunto(s)
Palabras clave
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Factor XII / Pyroglyphidae / Deficiencia del Factor XI / Hipersensibilidad Límite: Animals Idioma: En Revista: Am J Physiol Lung Cell Mol Physiol Asunto de la revista: BIOLOGIA MOLECULAR / FISIOLOGIA Año: 2017 Tipo del documento: Article Pais de publicación: Estados Unidos
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Factor XII / Pyroglyphidae / Deficiencia del Factor XI / Hipersensibilidad Límite: Animals Idioma: En Revista: Am J Physiol Lung Cell Mol Physiol Asunto de la revista: BIOLOGIA MOLECULAR / FISIOLOGIA Año: 2017 Tipo del documento: Article Pais de publicación: Estados Unidos