PMID: 18360088Mar 25, 2008Paper

Progress in allergy signal research on mast cells: regulation of allergic airway inflammation through toll-like receptor 4-mediated modification of mast cell function

Journal of Pharmacological Sciences
Masakatsu Yamashita, Toshinori Nakayama

Abstract

In a mouse experimental asthma model, the administration of bacterial lipopolysaccharide (LPS), particularly at low doses, enhances the levels of ovalbumin (OVA)-induced eosinophilic airway inflammation. In an effort to clarify the cellular and molecular basis for the LPS effect, we demonstrate that the OVA-induced eosinophilic inflammation in the lung is dramatically increased by administration of LPS at the priming phase in wild-type mice, whereas such an increase was not observed in mast cell deficient mice. Adoptive transfer of bone marrow-derived mast cells (BMMC) from wild type but not from Toll-like receptor 4 (TLR4)-deficient mice restored the increased eosinophilic inflammation in mast cell-deficient mice. Moreover, in vitro analysis revealed that treatment of BMMC with LPS resulted in sustained up-regulation of GATA1 expression and increased production of Th2 cytokines (IL-4, IL-5, and IL-13) upon restimulation. Thus, mast cells appear to control allergic airway inflammation after their activation and modulation through TLR4-mediated induction of GATA1 proteins and subsequent increase in Th2 cytokine production.

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Citations

Nov 28, 2013·American Journal of Respiratory Cell and Molecular Biology·Christoph TabelingMartin Witzenrath
May 13, 2010·The American Journal of the Medical Sciences·YuanYuan DingSiwang Wang
Oct 17, 2012·Vascular Pharmacology·Ali NaviJanice Tsui
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Apr 30, 2016·Allergy, Asthma & Immunology Research·Jun Pyo ChoiYoon Keun Kim
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Jun 15, 2019·International Journal of Molecular Sciences·Sun-Young Kwon, Jae-Hong Kim
Mar 14, 2018·Molecular Medicine Reports·Kyung-Ah ChoKyung Ho Lee

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