Progress in allergy signal research on mast cells: regulation of allergic airway inflammation through toll-like receptor 4-mediated modification of mast cell function
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.
The biologic activity of mast cell granules in rat skin: effects of adrenocorticosteroids on late-phase inflammatory responses induced by mast cell granules
Modification of the inflammatory response to allergen challenge after exposure to bacterial lipopolysaccharide
Identification of a conserved GATA3 response element upstream proximal from the interleukin-13 gene locus.
Lipopolysaccharide-enhanced, toll-like receptor 4-dependent T helper cell type 2 responses to inhaled antigen
GATA-1 as a regulator of mast cell differentiation revealed by the phenotype of the GATA-1low mouse mutant
Identification of specific gene expression profiles in human mast cells mediated by Toll-like receptor 4 and FcepsilonRI.
CD28 costimulation controls histone hyperacetylation of the interleukin 5 gene locus in developing th2 cells.
Regulation of allergic airway inflammation through Toll-like receptor 4-mediated modification of mast cell function
Nucleotide oligomerization domain 1 ligation suppressed murine allergen-specific T-cell proliferation and airway hyperresponsiveness
Omega-3 fatty acids suppress Th2-associated cytokine gene expressions and GATA transcription factors in mast cells
Lipopolysaccharide (LPS) exposure differently affects allergic asthma exacerbations and its amelioration by intranasal curcumin in mice
Diverse effects of bacterial cell wall components on mast cell degranulation, cysteinyl leukotriene generation and migration
Lipopolysaccharide/TLR4 Stimulates IL-13 Production through a MyD88-BLT2-Linked Cascade in Mast Cells, Potentially Contributing to the Allergic Response
House Dust Mite-Derived Chitin Enhances Th2 Cell Response to Inhaled Allergens, Mainly via a TNF-α-Dependent Pathway
Propofol Attenuates Airway Inflammation in a Mast Cell-Dependent Mouse Model of Allergic Asthma by Inhibiting the Toll-like Receptor 4/Reactive Oxygen Species/Nuclear Factor κB Signaling Pathway
This feed focuses in Asthma in which your airways narrow and swell. This can make breathing difficult and trigger coughing, wheezing and shortness of breath.
Allergy and Asthma
Allergy and asthma are inflammatory disorders that are triggered by the activation of an allergen-specific regulatory t cell. These t cells become activated when allergens are recognized by allergen-presenting cells. Here is the latest research on allergy and asthma.