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FcεR(1)-Mediated Mast Cell Reactivity Is Amplified through Prolonged Toll-Like Receptor-Ligand Treatment

BACKGROUND: Mast cell-derived mediators mediate several of the pathological features of asthma. Microbial infections induce asthma exacerbations in which the contribution of mast cells remains incomprehensible. PRINCIPAL FINDINGS: In this study we have investigated the characteristic expression patt...

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Autores principales: Saluja, Rohit, Delin, Ingrid, Nilsson, Gunnar P., Adner, Mikael
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3420882/
https://www.ncbi.nlm.nih.gov/pubmed/22916277
http://dx.doi.org/10.1371/journal.pone.0043547
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author Saluja, Rohit
Delin, Ingrid
Nilsson, Gunnar P.
Adner, Mikael
author_facet Saluja, Rohit
Delin, Ingrid
Nilsson, Gunnar P.
Adner, Mikael
author_sort Saluja, Rohit
collection PubMed
description BACKGROUND: Mast cell-derived mediators mediate several of the pathological features of asthma. Microbial infections induce asthma exacerbations in which the contribution of mast cells remains incomprehensible. PRINCIPAL FINDINGS: In this study we have investigated the characteristic expression pattern of Toll-like receptors (TLRs) 1–9 and the effect of TLR ligand treatment on IgE-receptor mediated mast cell reactivity. For the studies we employed in vitro differentiated connective tissue like mast cells (CTLMC) and mucosal like mast cells (MLMC) from mice. Both phenotypes were treated for 24 h or 96 h with ligands for TLR1/2, TLR2/6, TLR3 and TLR4, before activation with IgE and antigen. Prolonged exposure (96 h) with TLR-ligands promoted mast cell reactivity following IgE-receptor activation. TLR4 activation with LPS generated the most pronounced effect, with an enhanced degranulation and secretion of leukotrienes, cytokines and chemokines, in both CTLMC and MLMC. The effect of LPS was mediated through a Myd88-dependent pathway and the increased effect involved JNK-dependent pathway. CONCLUSION: We find that prolonged exposure of mast cells to pathogens/TLR-ligands modulates their effector responses by priming them for increased release of several inflammatory mediators when subsequently activated by IgE-receptors. These data suggest that infections might exaggerate the severity of allergic reactions such as in asthma, by enhancing mediator release from mast cells.
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spelling pubmed-34208822012-08-22 FcεR(1)-Mediated Mast Cell Reactivity Is Amplified through Prolonged Toll-Like Receptor-Ligand Treatment Saluja, Rohit Delin, Ingrid Nilsson, Gunnar P. Adner, Mikael PLoS One Research Article BACKGROUND: Mast cell-derived mediators mediate several of the pathological features of asthma. Microbial infections induce asthma exacerbations in which the contribution of mast cells remains incomprehensible. PRINCIPAL FINDINGS: In this study we have investigated the characteristic expression pattern of Toll-like receptors (TLRs) 1–9 and the effect of TLR ligand treatment on IgE-receptor mediated mast cell reactivity. For the studies we employed in vitro differentiated connective tissue like mast cells (CTLMC) and mucosal like mast cells (MLMC) from mice. Both phenotypes were treated for 24 h or 96 h with ligands for TLR1/2, TLR2/6, TLR3 and TLR4, before activation with IgE and antigen. Prolonged exposure (96 h) with TLR-ligands promoted mast cell reactivity following IgE-receptor activation. TLR4 activation with LPS generated the most pronounced effect, with an enhanced degranulation and secretion of leukotrienes, cytokines and chemokines, in both CTLMC and MLMC. The effect of LPS was mediated through a Myd88-dependent pathway and the increased effect involved JNK-dependent pathway. CONCLUSION: We find that prolonged exposure of mast cells to pathogens/TLR-ligands modulates their effector responses by priming them for increased release of several inflammatory mediators when subsequently activated by IgE-receptors. These data suggest that infections might exaggerate the severity of allergic reactions such as in asthma, by enhancing mediator release from mast cells. Public Library of Science 2012-08-16 /pmc/articles/PMC3420882/ /pubmed/22916277 http://dx.doi.org/10.1371/journal.pone.0043547 Text en © 2012 Saluja et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
spellingShingle Research Article
Saluja, Rohit
Delin, Ingrid
Nilsson, Gunnar P.
Adner, Mikael
FcεR(1)-Mediated Mast Cell Reactivity Is Amplified through Prolonged Toll-Like Receptor-Ligand Treatment
title FcεR(1)-Mediated Mast Cell Reactivity Is Amplified through Prolonged Toll-Like Receptor-Ligand Treatment
title_full FcεR(1)-Mediated Mast Cell Reactivity Is Amplified through Prolonged Toll-Like Receptor-Ligand Treatment
title_fullStr FcεR(1)-Mediated Mast Cell Reactivity Is Amplified through Prolonged Toll-Like Receptor-Ligand Treatment
title_full_unstemmed FcεR(1)-Mediated Mast Cell Reactivity Is Amplified through Prolonged Toll-Like Receptor-Ligand Treatment
title_short FcεR(1)-Mediated Mast Cell Reactivity Is Amplified through Prolonged Toll-Like Receptor-Ligand Treatment
title_sort fcεr(1)-mediated mast cell reactivity is amplified through prolonged toll-like receptor-ligand treatment
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3420882/
https://www.ncbi.nlm.nih.gov/pubmed/22916277
http://dx.doi.org/10.1371/journal.pone.0043547
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