Ontology highlight
ABSTRACT:
PROVIDER: PRJNA704504 | ENA |
REPOSITORIES: ENA
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Project description:Immunoglobulin (Ig) E-mediated activation of mast cells and basophils underlies allergic diseases such as asthma. Histamine-releasing factor (HRF), also known as translationally controlled tumor protein (TCTP) and fortilin, is a highly conserved protein with both intracellular and extracellular functions. Secreted HRF can stimulate histamine release and IL-4 and IL-13 production from IgE-sensitized basophils and mast cells. HRF is found in nasal, skin blister and bronchoalveolar lavage (BAL) fluids during late-phase allergic reactions (LPRs), which implicates HRF in the LPR and chronic allergic inflammation. Here we identify a subset of IgE and IgG antibodies as HRF-interacting molecules. HRF can exist as a dimer and bind to immunoglobulins (Igs) via interactions of its N-terminal and internal regions with the Fab region of Igs. Therefore, HRF together with HRF-reactive IgE can activate mast cells in vitro. The Ig-interacting HRF peptides that block HRF-Ig interactions can inhibit IgE+HRF-induced mast cell activation and in vivo cutaneous anaphylaxis and airway inflammation. Intranasally administered HRF can recruit inflammatory immune cells to the lung in naïve mice in a mast cell- and Fc receptor-dependent manner. These results strongly suggest the proinflammatory role of HRF in asthma and skin immediate hypersensitivity. A total of 6 samples were analyzed; wild type C57BL/6, FcRg KO and FceRIa KO mice were challenged with PBS (control) or mouse histamien-releasing factor
2011-12-04 | E-GEOD-34133 | biostudies-arrayexpress
Project description:CpG-oligodeoxynucleotides (CpG-ODNs) constitute an attractive alternative for asthma treatment. We found that free feeding of an ODNcap (a CpG-ODN-embedded particle) -containing feed (ODNcap-F) prophylactically attenuates allergic airway inflammation, hyperresponsiveness, and goblet cell hyperplasia in an ovalbumin (OVA) -induced asthma model. To seek the suppressive mechanism of action of ODNcap-F in OVA-induced airway insults, we analyzed the lung transcriptome using DNA microarray analysis.
2021-09-29 | GSE180287 | GEO
Project description:Mast cells, activated by antigen via the high affinity receptor for IgE (FcεRI), release an array of pro-inflammatory mediators that contribute to allergic disorders such as asthma and anaphylaxis. The KIT ligand, stem cell factor (SCF), is critical for mast cell expansion, differentiation and survival, and, under acute conditions, enhances mast cell activation. However, extended SCF exposure in vivo conversely protects against fatal antigen-mediated anaphylaxis. In investigating this dichotomy, we identified a novel mode of regulation of the mast cell activation phenotype through SCF-mediated programming. We found that mouse bone marrow-derived mast cells chronically exposed to SCF displayed a marked attenuation of FcεRI-mediated degranulation and cytokine production. The hypo-responsive phenotype was not a consequence of altered signals regulating calcium flux or protein kinase C, but of ineffective cytoskeletal reorganization, with evidence implicating a down-regulation of expression of the Src kinase Hck. Collectively, these findings demonstrate a major role for SCF in the homeostatic control of mast cell activation with potential relevance to mast cell-driven disease and the development of novel approaches for the treatment of allergic disorders. Mouse bone marrow-derived mast cells were treated with IL3, IL3+IL33, or IL3+SCF. Six replicates each.
2012-05-01 | E-GEOD-35332 | biostudies-arrayexpress
Project description:Immunoglobulin (Ig) E-mediated activation of mast cells and basophils underlies allergic diseases such as asthma. Histamine-releasing factor (HRF), also known as translationally controlled tumor protein (TCTP) and fortilin, is a highly conserved protein with both intracellular and extracellular functions. Secreted HRF can stimulate histamine release and IL-4 and IL-13 production from IgE-sensitized basophils and mast cells. HRF is found in nasal, skin blister and bronchoalveolar lavage (BAL) fluids during late-phase allergic reactions (LPRs), which implicates HRF in the LPR and chronic allergic inflammation. Here we identify a subset of IgE and IgG antibodies as HRF-interacting molecules. HRF can exist as a dimer and bind to immunoglobulins (Igs) via interactions of its N-terminal and internal regions with the Fab region of Igs. Therefore, HRF together with HRF-reactive IgE can activate mast cells in vitro. The Ig-interacting HRF peptides that block HRF-Ig interactions can inhibit IgE+HRF-induced mast cell activation and in vivo cutaneous anaphylaxis and airway inflammation. Intranasally administered HRF can recruit inflammatory immune cells to the lung in naïve mice in a mast cell- and Fc receptor-dependent manner. These results strongly suggest the proinflammatory role of HRF in asthma and skin immediate hypersensitivity.
2011-12-04 | GSE34133 | GEO
Project description:The objective of the study was to present a transcriptome-wide m6A methylome profile of lung tissues in mouse model of ovalbumin(OVA)-induced acute allergic asthma.
2021-10-11 | GSE179874 | GEO
Project description:TSLP is believed to play a role in allergic diseases such as atopic dermatitis and asthma, through its activation of dendritic cells which later promote the induction of inflammatory Th2 cells. We sought to characterize the inflammatory response induced by TSLP challenge in naive and OVA-sensitized mice using gene expression profiling.
2015-10-11 | GSE41667 | GEO
Project description:It is unknown how hypoxia exposure beginning at conception and maintained through adulthood, chronic developmental hypoxia (CDH), effects immune cell populations in the lung. This study utilized single cell RNA sequencing in a rat model of CDH combined with a model of OVA-induced asthma or a non-allergic model to assess the effect of CDH on lung immune cell populations in the context of allergic airway disease and in a non-allergic state.
2023-02-01 | GSE211925 | GEO
Project description:Oral immunotherapy (OIT) has been considered a promising approach for food allergies (FAs). However, the current OIT strategy is limited in terms of the long-term efficacy and safety. We have previously demonstrated that kakkonto, a traditional Japanese herbal medicine, suppresses the occurrence of allergic symptoms in a murine model of ovalbumin (OVA)-induced FA, which is attributed to the induction of the Foxp3+ CD4+ regulatory T cells. In this study, we established an OIT model using the FA mice with already established allergic symptoms and determined whether kakkonto could improve the efficacy of OIT. The OIT method consisted of initially administrating a very small amount of OVA and slowly increasing the amount. Allergic symptoms decreased in the OIT-treated FA mice. OIT significantly downregulated Th2 immune response-related gene expression in the FA mouse colon, and decreased a level of mouse mast cell protease-1, a marker of mast cell degranulation in the FA mouse plasma. Furthermore, the concomitant use of kakkonto significantly enhanced the effectiveness of OIT on the allergic symptoms, the Th2 immune responses and the mast cell degranulation in the OIT-treated FA mice. In addition, OIT significantly increased the population of Foxp3+ CD4+ regulatory T cells in the FA mouse colon, and this population was further increased by OIT in combination with kakkonto. Furthermore, the combined therapy with kakkonto reduced the expression of RA-degrading enzyme CYP26B1 mRNA in the FA mouse colon. These findings indicated that the combination of OIT with kakkonto represents a promising approach for FA treatment.
2016-12-29 | GSE92339 | GEO
Project description:Background: Inhalation exposure to biological particulate matter (BioPM) from livestock farms may provoke exacerbations in subjects suffering from allergy and asthma. The aim of this study was to use a murine model of allergic asthma to determine the effect of BioPM derived from goat farm on airway allergic responses Methods: Fine (< 2.5 μm) BioPM was collected from an indoor goat stable. Female BALB/c mice were ovalbumin (OVA) sensitized and challenged with OVA or saline as control. The OVA and saline groups were divided in sub-groups and exposed intranasally to different concentrations (0, 0.9, 3, or 9 μg) of goat farm BioPM. Bronchoalveolar lavage fluid (BALF), blood and lung tissues were collected. Results: In saline-challenged mice, goat farm BioPM alone induced a dose-dependent increase in neutrophils in BALF and induced production of macrophage inflammatory protein-3a). In OVA-challenged mice, BioPM significantly enhanced 1) inflammatory cells in BALF, 2) OVA-specific Immunoglobulin (Ig)G1, 3) interleukin-23 production, 4) airway mucus secretion-specific gene expression. RNAseq analysis of lungs indicates that neutrophil chemotaxis and oxidation-reduction processes were the representative genomic pathways in saline and OVA-challenged mice, respectively. Conclusions: A single exposure to goat farm BioPM enhanced airway inflammation in both saline and OVA-challenged allergic mice, with neutrophilic response as Th17 disorder and eosinophilic response as Th2 disorder indicative of the severity of allergic responses. Identification of the mode of action by which farm PM interacts with airway allergic pathways will be useful to design potential therapeutic approaches.
2020-08-01 | GSE148240 | GEO