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Lipocalin 2 modulates dendritic cell activity and shapes immunity to influenza in a microbiome dependent manner

ABSTRACT: Lipocalin 2 modulates dendritic cell activity and shapes immunity to influenza in a microbiome dependent manner

PROVIDER: PRJNA656717 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12433323.fastq.gz	Fastqsanger.gz
	SRR12433324.fastq.gz	Fastqsanger.gz
	SRR12433325.fastq.gz	Fastqsanger.gz
	SRR12433326.fastq.gz	Fastqsanger.gz
	SRR12433327.fastq.gz	Fastqsanger.gz

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Lipocalin 2 modulates dendritic cell activity and shapes immunity to influenza in a microbiome dependent manner

Project description:Lipocalin 2 (LCN2) is a secreted glycoprotein with roles in multiple biological processes. It contributes to host defense by interference with bacterial iron uptake and exerts immunomodulatory functions in various diseases. Here, we aimed to characterize the function of LCN2 in lung macrophages and dendritic cells (DCs) using Lcn2-deficient mice. Transcriptome analysis revealed strong LCN2-related effects in CD103+ DCs during homeostasis, with differential regulation of antigen processing and presentation and antiviral immunity pathways. We next validated the relevance of LCN2 in a mouse model of influenza infection, wherein LCN2 protected from excessive weight loss and improved survival. LCN2-deficiency was associated with enlarged mediastinal lymph nodes and increased lung T cell numbers, indicating a dysregulated immune response to influenza infection. In vivo T cell chimerism and in vitro T cell proliferation assays indicated that improved antigen processing by CD103+ DCs, rather than T cell intrinsic effects of LCN2, contribute to the exacerbated T cell response. Considering the antibacterial potential of LCN2 and that commensal microbes can modulate antiviral immune responses, we speculated that LCN2 might cause the observed influenza phenotype via the microbiome. Comparing the lung and gut microbiome of WT and Lcn2-/- mice by 16S rRNA gene sequencing, we observed profound effects of LCN2 on gut microbial composition. Interestingly, antibiotic treatment or co-housing of WT and Lcn2-/- mice prior to influenza infection equalized lung CD8+ T cell counts, suggesting that the LCN2-related effects are mediated by the microbiome. In summary, our results highlight a novel regulatory function of LCN2 in the modulation of antiviral immunity.

2021-04-02 | GSE156079 | GEO

Lipocalin 2 modulates dendritic cell activity and shapes immunity to influenza in a microbiome dependent manner.

Project description:Lipocalin 2 (LCN2) is a secreted glycoprotein with roles in multiple biological processes. It contributes to host defense by interference with bacterial iron uptake and exerts immunomodulatory functions in various diseases. Here, we aimed to characterize the function of LCN2 in lung macrophages and dendritic cells (DCs) using Lcn2-/- mice. Transcriptome analysis revealed strong LCN2-related effects in CD103+ DCs during homeostasis, with differential regulation of antigen processing and presentation and antiviral immunity pathways. We next validated the relevance of LCN2 in a mouse model of influenza infection, wherein LCN2 protected from excessive weight loss and improved survival. LCN2-deficiency was associated with enlarged mediastinal lymph nodes and increased lung T cell numbers, indicating a dysregulated immune response to influenza infection. Depletion of CD8+ T cells equalized weight loss between WT and Lcn2-/- mice, proving that LCN2 protects from excessive disease morbidity by dampening CD8+ T cell responses. In vivo T cell chimerism and in vitro T cell proliferation assays indicated that improved antigen processing by CD103+ DCs, rather than T cell intrinsic effects of LCN2, contribute to the exacerbated T cell response. Considering the antibacterial potential of LCN2 and that commensal microbes can modulate antiviral immune responses, we speculated that LCN2 might cause the observed influenza phenotype via the microbiome. Comparing the lung and gut microbiome of WT and Lcn2-/- mice by 16S rRNA gene sequencing, we observed profound effects of LCN2 on gut microbial composition. Interestingly, antibiotic treatment or co-housing of WT and Lcn2-/- mice prior to influenza infection equalized lung CD8+ T cell counts, suggesting that the LCN2-related effects are mediated by the microbiome. In summary, our results highlight a novel regulatory function of LCN2 in the modulation of antiviral immunity.

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Lipocalin-2 deficiency attenuates acute lung inflammation

Project description:Lipocalin-2 promotes acute lung inflammation

2023-02-28 | GSE198406 | GEO

Ultraviolet radiation shapes dendritic cell leukaemia transformation in the skin

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STAT5 and STAT3 balance shapes dendritic cell function and tumor immunity

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Maternal dietary fat during lactation shapes single nucleus transcriptomic profile of postnatal offspring hypothalamus in a sexually dimorphic manner in mice

Project description:Maternal overnutrition during pregnancy/or lactation predisposes offspring obesity and related metabolic syndromes in later life. Hypothalamus is the highest heterogeneous brain region located at the base of the brain that is critical to the regulation of the energy homeostasis.We investigated how the maternal programming shapes the single-nucleus transcriptomic landscapes in postnatal day15 offspring hypothalamus in a sex-specific manner.

2024-02-18 | GSE217677 | GEO

Adipose-Derived Lipocalin-2 Causes Metabolic Dysfunction Only in Female Mice

Project description:Lipocalin-2 (LCN2) is a secreted protein involved in innate immunity and also has been associated with several cardiometabolic traits. We examined LCN2 expression in a panel of diverse inbred mouse strains and observed a striking sex difference. Adipose LCN2 was associated with obesity, insulin resistance, dyslipidemia, and hepatic steatosis in females but not males. We expressed LCN2 either in adipose or liver in a tissue specific manner on the background of a whole-body knockout mouse. Adipose LCN2 expression, acting in an autocrine/paracrine manner, promoted metabolic disturbances in females but not males, whereas liver LCN2 expression had no impact on the traits examined. The adipose expression was accompanied by adipose inflammation, fibrosis, and mitochondrial dysfunction, contributing in part to the metabolic disorders. We also show that LCN2 inversely regulates its receptor, LRP2 (or megalin), in a sex-specific manner. Our results demonstrate striking sex- and tissue- specific functions of LCN2.

2018-10-11 | GSE121098 | GEO

IL-21 Shapes the B Cell Response in a Context-Dependent Manner [CUT&RUN]

Project description:IL-21 Shapes the B Cell Response in a Context-Dependent Manner [CUT&RUN]

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IL-21 Shapes the B Cell Response in a Context-Dependent Manner [RNA-seq

Project description:IL-21 Shapes the B Cell Response in a Context-Dependent Manner [RNA-seq

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IFN lambda modulates dendritic cells to facilitate T cell immunity during influenza virus infection

Project description:Type I and type III interferon (IFN) are important in regulating responses to viral infection. Type I IFN signaling is know to contribute to dendritic cell (DC) function, but the contribution of type III IFN remains unknown. To determine changes in migratory dendritic cell gene expression during influenza A virus (IAV) in the presence or absence of type I or type III (IFN) receptors, C57Bl/6 (WT) mice, mice lacking the type I IFN receptor (Ifnar-/-), and mice lacking the type III IFN receptor (Ifnlr-/-) were infected intranasally with 40 plaque forming units (PFU) IAV H1N1 strain A/PR/8/34 or mock infected. On day 4, lung-draining lymph nodes (dLN) were harvested, conventional DC were isolated, and mRNA sequencing (mRNAseq) was performed.

2018-12-28 | GSE124399 | GEO

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