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

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

PROVIDER: PRJNA765664 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16027125.fastq.gz	Fastqsanger.gz
	SRR16027126.fastq.gz	Fastqsanger.gz
	SRR16027127.fastq.gz	Fastqsanger.gz
	SRR16027128.fastq.gz	Fastqsanger.gz
	SRR16027129.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

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

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

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

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Type-I interferon priming signal balances anti-bacterial and anti-tumor trained immunity in alveolar macrophages [RNA-seq]

Project description:Tissue-resident macrophages may be trained to confer enhanced response to heterologous re-stimulation, and thus foster versatile trained immunity (TI) against both infections and tumors. However, key priming signals that contribute to such functional versatility in trained macrophages remain not fully understood. Here we show that influenza A virus (IAV) infection in mice induces lasting transcriptional imprints of acute type-I interferon (IFN-I) signaling in lung-resident alveolar macrophages (AMs) that confer balanced anti-bacterial and anti-tumor TI responses. In both IAV-infected mice and an ex vivo cytokine-mediated training system, IFN-I signaling is found to be critical to developing anti-tumor TI functions, although it limits anti-bacterial TI functions in AMs. Moreover, human AMs carrying transcriptional imprints of IFN-I signaling are associated with anti-tumor immunity and immune activation in lung cancer tissues. Our findings highlight IFN-I as a key priming signal required to developing versatile TI functions in AMs with balanced anti-bacterial and anti-tumor potential.

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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.

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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.

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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.

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