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Multi-omics profiling reveals microenvironmental remodeling as a key driver of house dust mite-induced lung cancer progression

ABSTRACT: Chronic exposure to the common aeroallergen house dust mite (HDM) induces lung inflammation and DNA damage, but its impact on lung cancer development remains largely unexplored. Using whole-genome sequencing, RNA-seq, and DNA methylation profiling, we assessed HDM effects in lung epithelial cell lines and a mouse orthotopic lung cancer model. HDM accelerated tumor growth without altering mutational burden. Transcriptomic and epigenetic analyses revealed tissue-specific effects: in normal lung, HDM enhanced pro-inflammatory and immune activation programs, whereas in tumors it suppressed T cell responses, antigen presentation, and chemokine signaling. Immune deconvolution showed a shift toward myeloid enrichment and lymphoid suppression, with reduced cytotoxic T and NK signatures. Notably, HDM-driven tumor promotion was abolished in Il17a−/− but not Il1b−/− mice, identifying IL-17A as a critical mediator. These findings demonstrate that chronic aeroallergen exposure reshapes the lung microenvironment to promote immune suppression and accelerate lung cancer progression.

ORGANISM(S): Mus musculus

PROVIDER: GSE308855 | GEO | 2026/01/16

REPOSITORIES: GEO

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Multi-omics profiling reveals microenvironmental remodeling as a key driver of house dust mite-induced lung cancer progression

Project description:Chronic exposure to the common aeroallergen house dust mite (HDM) induces lung inflammation and DNA damage, but its impact on lung cancer development remains largely unexplored. Using whole-genome sequencing, RNA-seq, and DNA methylation profiling, we assessed HDM effects in lung epithelial cell lines and a mouse orthotopic lung cancer model. HDM accelerated tumor growth without altering mutational burden. Transcriptomic and epigenetic analyses revealed tissue-specific effects: in normal lung, HDM enhanced pro-inflammatory and immune activation programs, whereas in tumors it suppressed T cell responses, antigen presentation, and chemokine signaling. Immune deconvolution showed a shift toward myeloid enrichment and lymphoid suppression, with reduced cytotoxic T and NK signatures. Notably, HDM-driven tumor promotion was abolished in Il17a−/− but not Il1b−/− mice, identifying IL-17A as a critical mediator. These findings demonstrate that chronic aeroallergen exposure reshapes the lung microenvironment to promote immune suppression and accelerate lung cancer progression.

2026-01-22 | GSE317298 | GEO

A Single-cell Transcriptomic Profiling Reveals the Effects of Chronic House Dust Mite Exposure on the Murine Lung Microenvironment

Project description:House dust mite (HDM) is a common environmental aeroallergen linked to the development of allergic airway inflammation and asthma. While the effects of acute HDM exposure on T helper 2 (Th2)-driven allergic responses and pulmonary eosinophilia are well established in murine models, the impact of chronic HDM exposure on other inflammatory responses, particularly those involving interleukin-1β (IL-1β) and neutrophilia, remains poorly defined. To address this gap, we performed single-cell RNA sequencing (scRNA-seq) to examine lung immune responses in wild-type and IL-1β-deficient mice following chronic HDM exposure. Our data reveal that HDM promotes the recruitment of diverse immune cell populations in the lungs, including neutrophils, alternatively activated (M2-polarized) macrophages, B-2 (follicular) B cells, and multiple CD4 regulatory and effector T cell subsets. IL-1β signaling was essential for supporting neutrophil and Th17 responses, whereas its absence enhanced Th2-skewed immune polarization in the lung. These immune populations differently contribute to the development or resolution of lung inflammation in an IL-1β-dependent or -independent manner. This study offers a detailed characterization of the cellular and molecular alterations induced by chronic HDM exposure and reveals previously unrecognized roles for IL-1β in orchestrating chronic lung inflammation.

2025-10-29 | GSE300531 | GEO

Mouse skin CD45 cells in house dust mite dermatitis

Project description:Despite robust literature associating IL-31 with pruritic inflammatory skin diseases, its influence on cutaneous inflammation and on the interplay between inflammatory and neurosensory pathways remain unmapped. Here, we examined the consequences of disrupting Il31 and its receptor Il31ra in a mouse model of house dust mite (HDM) allergic dermatitis. Il31-deficient mice displayed an increased number and proportion of cutaneous type 2 cytokine-producing CD4 T cells and serum IgE in response to HDM. Single cell RNA-sequencing analysis of skin CD45+ populations from HDM-treated skin revealed that Il4ra+ monocytes and macrophages capable of fueling a feedforward type 2 inflammatory loop were selectively enriched in Il31ra-deficient HDM dermatitis skin. Thus, IL-31 is not strictly a pro-inflammatory cytokine, but rather an immunoregulatory factor that limits the magnitude of type 2 inflammatory responses in skin.

2023-10-26 | GSE236744 | GEO

Genome wide DNA methylation and Hydroxymethylation of F1 mouse lung prenatally exposed to house dust mite

Project description:We used a mouse model of allergic lung disease to examine the effects of pre- and perinatal house dust mite (HDM) allergen exposure on offspring lung phenotypic and transcriptional outcomes. We showed that maternal HDM exposure (F0) acts synergistically with adult HDM exposure, leading to enhanced airway hyperresponsiveness (AHR) and lung inflammation when compared to mice exposed solely in adulthood. To examine the role of epigenetic inheritance of asthma susceptibility induced by maternal HDM exposure, we utilized a genome-wide MeDIP-seq and hMeDIP-seq analysis to identify genes differentially methylated (DMG) and hydroxymethylated (DHG), and their association with the enhanced AHR. In addition, we validated the relationship between DNA methylation and mRNA expression of the DMGs and DHGs in the male progenies.

2021-03-23 | GSE169355 | GEO

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Project description:We examined the transcriptional changes in mouse lungs induced by house dust mite (HDM), D.f. extract and the isolated RNA was utilized for RNA-seq analysis. Our results demonstrated that HDM strongly triggered an inflammatory response.

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IL-22 inhibits allergic airway inflammation in house dust mite-induced asthma models

Project description:While the pathogenesis of asthma is mainly orchestrated by antigen-specific Th2 cells and their cytokines, recent findings indicate the involvement of other subsets of helper T cells including Th17 cells. Previous studies have shown that IL-22, one of Th17 cell-related cytokines, plays multiple roles in regulating allergic airway inflammation; however, the mechanism underlying the Il-22-mediated regulation remains unclear. Here, we show that allergic airway inflammation upon intratracheal administration of house dust mite extract (HDM), a representative allergen, were exacerbated in IL-22-deficient mice. To address the molecular mechanisms by which IL-22 inhibits the development of HDM-induced allergic airway inflammation, we next performed an unbiased comprehensive screening of genes induced by IL-22 administration in the lung by RNA-seq analysis.

2017-08-10 | GSE100858 | GEO

Effects of endotoxin abundance in house dust mite on the molecular phenotype of inflammation and tissue response in mouse lung

Project description:We report that the abundance of endotoxin in commercially available house dust mite extracts significantly alters the lung transcriptome and secretome in a mouse model of allergic asthma. Studies using the HDM model of asthma in mice should consider reporting the abundance of endotoxin in their commercial HDM stocks in an effort to standardize the protocols and to facilitate consistant and reliable comparison between different studies.

2020-07-15 | GSE116967 | GEO

Gene expression patterns in house dust mite stimulated CD4 T cells and IgG:IgE ratios

Project description:PBMC from house dust mite (HDM) sensitized atopics were cultured in the presence or absence of HDM extract for 24 hours. At the termination of the cultures, CD4 T cells were isolated using immunomagnetic separation. Gene expression was profiled on microarrays. The study design consisted of 45 subjects and two conditions (medium control, HDM stimulation).

2015-11-03 | E-GEOD-70760 | biostudies-arrayexpress

Gene expression patterns in house dust mite stimulated CD4 T cells and IgG:IgE ratios

2015-11-03 | GSE70760 | GEO

Shifting of immune responsiveness to house dust mite by influenza a infection genomic insights

Project description:House dust mite (HDM) extract (Greer Laboratories, Lenoir, NC) was resuspended in sterile phosphate-buffered saline (PBS) at a concentration of 0.5 mg (protein)/ml and 10 ul (5 ug dose) was administered to isofluorane-anesthetized mice intranasally. Groups of mice were infected either with influenza A or exposed to PBS. Seven days later, separate groups of mice were either exposed to saline or HDM for 3 or 6 days and lungs harvested 24 h after the last exposure, at day 4 (early phase; EP) or day 7 (late phase; LP).

2011-08-16 | E-MEXP-3325 | biostudies-arrayexpress

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