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An IL-9-pulmonary macrophage axis defines the allergic lung inflammatory environment

ABSTRACT: An IL-9-pulmonary macrophage axis defines the allergic lung inflammatory environment

PROVIDER: PRJNA683661 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13221443_1.fastq.gz	Fastqsanger.gz
	SRR13221443_2.fastq.gz	Fastqsanger.gz
	SRR13221444_1.fastq.gz	Fastqsanger.gz
	SRR13221444_2.fastq.gz	Fastqsanger.gz
	SRR13221445_1.fastq.gz	Fastqsanger.gz

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An IL-9-pulmonary macrophage axis defines the allergic lung inflammatory environment

Project description:Despite IL-9 functioning as a pleiotropic cytokine in mucosal environments, the IL-9 responsive cell repertoire is still not well defined. Here, we found IL-9 mediates pro-allergic activities by targeting lung macrophages. IL-9 inhibits alveolar macrophage expansion and promotes recruitment of monocytes that develop into CD11c+/- interstitial macrophage populations. Interstitial macrophages were required for IL-9-dependent allergic responses. Mechanistically, IL-9 affects the function of lung macrophages by inducing Arg1 activity. Compared to Arg1-deficient lung macrophages, Arg1-expressing macrophages co-express greater amounts of CCL5. Adoptive transfer of Arg1+ lung macrophages but not Arg1- lung macrophages can recover allergic inflammation that is lost in Il9r-/- mice. In parallel, the elevated expression of IL-9, IL-9R, Arg1 and CCL5 is correlated with disease in asthma patients. Thus, our study uncovers an IL-9/macrophage/Arg1 axis as a potential therapeutic target for allergic airway inflammation.

2021-11-15 | GSE162898 | GEO

An IL-9-pulmonary macrophage axis defines the allergic lung inflammatory environment.

Project description:Despite IL-9 functioning as a pleiotropic cytokine in mucosal environments, the IL-9-responsive cell repertoire is still not well defined. Here, we found that IL-9 mediates proallergic activities in the lungs by targeting lung macrophages. IL-9 inhibits alveolar macrophage expansion and promotes recruitment of monocytes that develop into CD11c+ and CD11c- interstitial macrophage populations. Interstitial macrophages were required for IL-9-dependent allergic responses. Mechanistically, IL-9 affected the function of lung macrophages by inducing Arg1 activity. Compared with Arg1-deficient lung macrophages, Arg1-expressing macrophages expressed greater amounts of CCL5. Adoptive transfer of Arg1+ lung macrophages but not Arg1- lung macrophages promoted allergic inflammation that Il9r-/- mice were protected against. In parallel, the elevated expression of IL-9, IL-9R, Arg1, and CCL5 was correlated with disease in patients with asthma. Thus, our study uncovers an IL-9/macrophage/Arg1 axis as a potential therapeutic target for allergic airway inflammation.

| S-EPMC8991419 | biostudies-literature

Altered response of macrophages to an inflammatory stimulus in an allergic environment

Project description:To investigate how an allergic cytokine environment (associated with increased levels of IL4 and IL-13) alters the response of macrophages to a pro-inflammatory stimulus.

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TERT expression defines clinical outcome in pulmonary carcinoids

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The covariance environment defines cellular niches for spatial inference

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The USP7-STAT3-granzyme-Par-1 axis regulates allergic inflammation by promoting differentiation of IL-5-producing Th2 cells

Project description:Uncontrolled type 2 immunity by type 2 helper T (Th2) cells causes intractable allergic diseases; however, whether the interaction of CD4+ T cells shapes the pathophysiology of allergic diseases remains unclear. We identified a subset of Th2 cells that produced the serine proteases granzyme A and B early in differentiation. Granzymes cleave protease-activated receptor (Par)-1 and induce phosphorylation of p38 mitogen-activated protein kinase (MAPK), resulting in the enhanced production of IL-5 and IL-13 in both mouse and human Th2 cells. Ubiquitin-specific protease 7 (USP7) regulates IL-4-induced phosphorylation of STAT3, resulting in granzyme production during Th2 cell differentiation. Genetic deletion of Usp7 or Gzma and pharmacological blockade of granzyme B ameliorated allergic airway inflammation. Furthermore, PAR-1+ and granzyme+ Th2 cells were colocalized in nasal polyps from patients with eosinophilic chronic rhinosinusitis. Thus, the USP7-STAT3-granzymes-Par-1 pathway is a potential therapeutic target for intractable allergic diseases.

2023-11-13 | GSE229875 | GEO

Altered response of macrophages to an inflammatory stimulus in an allergic environment

Project description:Altered response of macrophages to an inflammatory stimulus in an allergic environment

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IL-33/IL-31 Axis in Immune-Mediated and Allergic Diseases.

Project description:Several allergic and immunologic diseases including asthma, food allergy (FA), chronic spontaneous urticaria (CSU), atopic dermatitis (AD), systemic lupus erythematosus (SLE), systemic sclerosis (SSc), rheumatoid arthritis (RA), and Behçet's disease (BD) are characterized by the involvement of Th2 immunity. Several mediators lead to immunoglobulin (Ig)E production, thus including key cytokines such as interleukin (IL)-4, IL-5, and IL-13. Among them, IL-31 and IL-33 have been recently studied as novel biomarkers and future therapeutic targets for allergic and immunological disorders. IL-31 is a proinflammatory cytokine-it regulates cell proliferation and is involved in tissue remodeling. IL-33, acting through its receptor suppression of tumorigenity (ST2L), is an alarmin cytokine from the IL-1 family, whose expression is mediated by tissue damage. The latter has a pleiotropic effect, as it may modulate specific and innate immune cells functions. To date, several researchers have investigated the involvement of IL-31 and IL-33 in several allergic and immune-mediated diseases. Further studies are needed to understand the future applications of these molecules as novel therapeutic agents. This paper aims to give the readers a complete and updated review of IL-31 and IL-33 involvement among the most common autoimmune and allergic disorders.

| S-EPMC6929191 | biostudies-literature

Mgl2+ cDC2s coordinate allergic airway type 2 but not type 17 inflammation against fungal spores

Project description:Fungal spores, abundant in the environment, are a major cause of asthma. But the precise host response that triggers fungal allergic airway inflammation remains unclear. We found that CD11c+ DCs and CD4+ T cells are essential for development of airway inflammation in mice when repeatedly exposed to inhaled spores. To delinate which DC subsets are mediating fungal allergic inflammation we undertook single cell RNAseq of DCs isolated from the lungs of mice exposed to fungal spores. This identified precise subsets altered upon spore exposure and following targeted removal identified distinct DC subsets (Mgl2+ cDC2s) that are essential for fungal allergic airway inflammation.

2024-12-04 | E-MTAB-13740 | biostudies-arrayexpress

TLR9-IL-2 axis exacerbates allergic asthma by preventing IL-17A hyperproduction.

Project description:Allergic asthma is one of most famous allergic diseases, which develops lung and airway inflammation. Recent studies have revealed the relationship between the pathology of allergic asthma and the increase of host-derived DNA in inflamed lung, but the role of the DNA-recognizing innate immune receptor for the inflammation is unknown well. Here we investigated the role of Toll-Like Receptor 9 in the pathogenesis of allergic asthma without synthesized CpG-ODNs. To examine that, we analyzed the pathology and immunology of house-dust-mite (HDM)-induced allergic asthma in Tlr9-/- mice and TLR9-inhibitory-antibody-treated mice. In Tlr9-/- mice, airway hyperresponsiveness (AHR) and the number of eosinophils decreased, and production of the Th2 cytokines IL-13, IL-5, and IL-4 was suppressed, compared with in wild-type mice. Interestingly, unlike Th2 cytokine production, IL-17A production was increased in Tlr9-/- mice. Furthermore, production of IL-2, which decreases IL-17A production, was reduced in Tlr9-/- mice. Blockade of TLR9 by treatment with TLR9-inhibitory-antibody, NaR9, effectively suppressed the development of allergic asthma pathology. IL-17A production in NaR9-treated mice was enhanced, which is comparable to Tlr9-/- mice. These results suggest that the TLR9-IL-2 axis plays an important role in Th2 inflammation by modulating IL-17A production in HDM-induced allergic asthma and that targeting of TLR9 might be a novel therapeutic method for allergic asthma.

| S-EPMC7581806 | biostudies-literature

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