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Multiplexed transcriptional profiling to Dermatophagoides House Dust Mites allergens in human epithelium cells

ABSTRACT: Allergic asthma, a chronic disease-causing inflammation in the airways, is a significant public health concern. Our research team discovered that more than 80% of allergic children in central Taiwan were sensitized to various house dust mites (HDMs). This investigation focuses on how the crude extracts of HDMs affect human epithelium BEAS-2B cells to understand the early fundamental mechanisms for preventing allergic diseases. Therefore, RNA-seq analysis revealed that three Dermatophagoides HDMs allergens activate a common Toll-like receptor signaling pathway in human epithelial cells within a 4-hour treatment. During this process, the nuclear transcription factor NF-κB translocated into the cell nucleus within 30 minutes of allergen stimulation, triggering the expression of pro-inflammatory genes such as IL-6 and IL-8 over 4 hours. Additionally, treating the cells with specific Dermatophagoides microceras (Der m) allergens, there was an upregulation of genes in regulating type 1 diabetes mellitus signaling pathways, mediating IL-12A inflammation. Moreover, an increase in gene sets related to cilia function and the microtubule cytoskeleton in human epithelial cells following treatment combined with Der m allergens and Dexamethasone. Furthermore, OMICs analysis investigates the effects of HDMs allergenic stimulation on the human epidermal cells. This process aims to enhance our understanding of the cellular molecular mechanisms underlying potential targets and bioactive substances in precision medicine for treating asthma caused by HDMs allergens.

ORGANISM(S): Homo sapiens

PROVIDER: GSE243680 | GEO | 2023/12/31

REPOSITORIES: GEO

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Mass spectrometry analysis of cleavage sites for different protease allergens in human IL-33

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2018-03-14 | PXD006081 | Pride

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Project description:Group 2 innate lymphoid cells (ILC2s) in the lung are stimulated by inhaled allergens. ILC2s do not directly recognize allergens but they are stimulated by cytokines including interleukin (IL)-33 released by damaged epithelium.Lung ILC2s, upon stimulation, produce T helper 2 cell-type cytokines inducing T cell independent allergic lung inflammation. We now report that lung ILC2s, upon activation by an allergen or IL-33, acquire the properties of memory cells. The activated ILC2s initially proliferate and secrete cytokines, followed by a contraction phase as they stop producing cytokines. Nevertheless, some persist long after the resolution of the inflammation and acquire intrinsic capacities to react to unrelated allergens more vigorously than naÃ¯ve ILC2s, thus mediating a severe allergic lung inflammation. Gene expression profiles of the previously activated ILC2s show a gene signature of memory T cells. These antigen non-specific memory ILC2s may explain why asthma patients are often sensitized to multiple allergens. ILC2s were isolated from mouse lungs from naive and IL-33 injected mice 4 days, 14 days and 4 months after the initial treatment. RNA was extracted from those ILC2 populations and analyzed for gene expression profiles. RNA was also extracted from ILC2s isolated from lung draining mediastinal lymph node (mLN) 4 days and 14 days after IL-33 treatment.

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2016-06-30 | GSE81700 | GEO

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