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Trained immunity of alveolar macrophages depends on metabolic rewiring and type 1 interferon signaling (ATAC-Seq)

ABSTRACT: Trained immunity of alveolar macrophages depends on metabolic rewiring and type 1 interferon signaling (ATAC-Seq)

PROVIDER: PRJNA765639 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16027116.fastq.gz	Fastqsanger.gz
	SRR16027117.fastq.gz	Fastqsanger.gz
	SRR16027118.fastq.gz	Fastqsanger.gz
	SRR16027119.fastq.gz	Fastqsanger.gz
	SRR16027120.fastq.gz	Fastqsanger.gz

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Trained immunity of alveolar macrophages depends on metabolic rewiring and type 1 interferon signaling

Project description:Trained immunity of alveolar macrophages depends on metabolic rewiring and type 1 interferon signaling

| PRJNA765644 | ENA

Trained immunity of alveolar macrophages depends on metabolic rewiring and type 1 interferon signaling (RNA-Seq)

Project description:Trained immunity of alveolar macrophages depends on metabolic rewiring and type 1 interferon signaling (RNA-Seq)

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Trained immunity of alveolar macrophages depends on metabolic rewiring and type 1 interferon signaling (RNA-Seq)

Project description:Environmental microbial triggers shape the development and functionality of the immune system. Alveolar macrophages (AMs), tissue-resident macrophages of the lungs, are in constant and direct contact with inhaled particles and microbes. Such exposures likely impact AM reactivity to subsequent challenges by immunological imprinting mechanisms referred to as trained immunity. Here, we investigated whether a ubiquitous microbial compound has the potential to induce AM training in vivo. We showed that intranasal exposure to ambient amounts of lipopolysaccharide (LPS) protected mice from bacterial pneumonia six days later and discovered a pronounced AM memory response, characterized by enhanced reactivity upon pneumococcal challenge. Exploring the mechanistic basis of AM training, we identified a critical role of type 1 interferon signaling and found that trained AMs displayed a substantially modulated metabolite and lipid composition. Inhibition of fatty acid oxidation and glutaminolysis significantly attenuated the training effect, suggesting a key function of metabolic rewiring in LPS-induced AM memory. Collectively, our findings demonstrate the profound impact of ambient microbial exposure on pulmonary immune memory and highlight tissue-specific features of trained immunity.

2022-07-18 | GSE184683 | GEO

Trained immunity of alveolar macrophages depends on metabolic rewiring and type 1 interferon signaling (ATAC-Seq)

2022-07-18 | GSE184682 | GEO

Trained immunity of alveolar macrophages requires metabolic rewiring and type 1 interferon signaling.

Project description:Environmental microbial triggers shape the development and functionality of the immune system. Alveolar macrophages (AMs), tissue-resident macrophages of the lungs, are in constant and direct contact with inhaled particles and microbes. Such exposures likely impact AM reactivity to subsequent challenges by immunological imprinting mechanisms referred to as trained immunity. Here, we investigated whether a ubiquitous microbial compound has the potential to induce AM training in vivo. We discovered that intranasal exposure to ambient amounts of lipopolysaccharide (LPS) induced a pronounced AM memory response, characterized by enhanced reactivity upon pneumococcal challenge. Exploring the mechanistic basis of AM training, we identified a critical role of type 1 interferon signaling and found that inhibition of fatty acid oxidation and glutaminolysis significantly attenuated the training effect. Notably, adoptive transfer of trained AMs resulted in increased bacterial loads and tissue damage upon subsequent pneumococcal infection. In contrast, intranasal pre-exposure to LPS promoted bacterial clearance, highlighting the complexity of stimulus-induced immune responses, which likely involve multiple cell types and may depend on the local immunological and metabolic environment. Collectively, our findings demonstrate the profound impact of ambient microbial exposure on pulmonary immune memory and reveal tissue-specific features of trained immunity.

| S-EPMC9385480 | biostudies-literature

Trained immunity of alveolar macrophages depends on metabolic rewiring and type 1 interferon signaling

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-07-18 | GSE184684 | GEO

Influenza-trained mucosal-resident alveolar macrophages confer long-term antitumor immunity in the lungs [RNA-seq]

Project description:Respiratory viral infections reprogram pulmonary macrophages with altered anti-infectious functions. However, the potential function of virus-trained macrophages in antitumor immunity in the lung, a preferential target of both primary and metastatic malignancies, is not well understood. Using mouse models of influenza and lung metastatic tumors, we show here that influenza trains respiratory mucosal-resident alveolar macrophages (AMs) to exert long-lasting and tissue-specific antitumor immunity. Trained AMs infiltrate tumor lesions and have enhanced phagocytic and tumor cell cytotoxic functions, which are associated with epigenetic, transcriptional and metabolic resistance to tumor-induced immune suppression. Generation of antitumor trained immunity in AMs is dependent on interferon-γ and natural killer cells. Notably, human AMs with trained immunity traits in non-small cell lung cancer tissue are associated with a favorable immune microenvironment. These data reveal a function for trained resident macrophages in pulmonary mucosal antitumor immune surveillance. Induction of trained immunity in tissue-resident macrophages might thereby be a potential antitumor strategy.

2023-01-09 | GSE222149 | GEO

Influenza-trained mucosal-resident alveolar macrophages confer long-term antitumor immunity in the lungs [ATAC-seq]

2023-01-09 | GSE222148 | GEO

Trained immunity of alveolar macrophages promotes injury resolution by enhancing KLF4-MERTK-mediated efferocytosis

Project description:Recent studies suggest that training of innate immune cells such as tissue-resident macrophages by repeated noxious stimuli can heighten host defense responses. However, it remains unclear whether trained immunity of tissue-resident macrophages also comprises enhanced injury resolution capacity to counterbalance the heightened inflammatory responses. Here, we studied lung-resident alveolar macrophages (AMs) pre-challenged with either the bacterial endotoxin or with Pseudomonas aeruginosa and observed that these trained AMs showed greater resilience to pathogen-induced cell death. Transcriptomic analysis, and functional assays showed greater capacity of trained AMs to efferocytosis of cellular- debris, and facilitate injury resolution. Single-cell high-dimensional mass-cytometry analysis and lineage tracing demonstrated that training induces an expansion of a MERTKhiMarcohiCD163+F4/80low lung-resident AMs subset with pro-resolving phenotypes. Training epigenetically reprogrammed AMs to express a higher level of the transcription factor KLF4 which in turn upregulates the efferocytosis receptor MERTK. Adoptive transfer of these trained AMs restricted inflammatory lung injury in recipient mice exposed to lethal Pseudomonas aeruginosa. Thus, our study has identified a unique subset of tissue-resident trained macrophages which prevent hyper-inflammation and restore tissue homeostasis following pathogen challenge.

2023-08-16 | GSE231217 | GEO

Hydroxychloroquine inhibits trained immunity

Project description:We demonstrate that hydroxychloroquine inhibits trained immunity at the functional and epigenetic level and is accompanied by reduced expression of interferon-stimulated genes. Trained immunity comprises a functional adaptation induced by epigenetic reprogramming which facilitates the anti-viral innate immune response.

2020-10-21 | GSE159678 | GEO

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