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lüll Progress in allergy signal research on mast cells: regulation of allergic airway inflammation through toll-like receptor 4-mediated modification of mast cell function Yamashita M; Nakayama TJ Pharmacol Sci 2008[Mar]; 106 (3): 332-5In 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.|Adoptive Transfer[MESH]|Animals[MESH]|Asthma/*etiology[MESH]|Cytokines/biosynthesis[MESH]|Eosinophilia/etiology[MESH]|GATA1 Transcription Factor/genetics[MESH]|GATA2 Transcription Factor/genetics[MESH]|Lipopolysaccharides/pharmacology[MESH]|Mast Cells/*physiology[MESH]|Th2 Cells/immunology[MESH]|Toll-Like Receptor 4/*physiology[MESH] |