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LAIR1 prevents excess inflammatory tissue damage in S. aureus skin infection and Cutaneous T-cell Lymphoma [abscess]

ABSTRACT: LAIR1 prevents excess inflammatory tissue damage in S. aureus skin infection and Cutaneous T-cell Lymphoma [abscess]

PROVIDER: PRJNA1120461 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29299732_1.fastq.gz	Fastqsanger.gz
	SRR29299732_2.fastq.gz	Fastqsanger.gz
	SRR29299733_1.fastq.gz	Fastqsanger.gz
	SRR29299733_2.fastq.gz	Fastqsanger.gz
	SRR29299734_1.fastq.gz	Fastqsanger.gz

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LAIR1 prevents excess inflammatory tissue damage in S. aureus skin infection and Cutaneous T-cell Lymphoma [abscess]

Project description:Patients with cutaneous T cell lymphoma (CTCL) experience high morbidity and mortality due to S. aureus skin infections and sepsis, but the causative immune defect is unclear. We propose that high levels of LAIR2 in CTCL suppress LAIR1 inhibitory signaling, promoting inflammation and tissue damage, which increases S. aureus susceptibility. Mice do not have a LAIR2 homolog, so we used Lair1 KO mice to model LAIR2 overexpression. In a model of subcutaneous S. aureus skin infection, Lair1 KO mice had significantly larger abscesses and areas of dermonecrosis compared to WT. Lair1 KO exhibited a pattern of increased inflammatory responses in infection and sterile immune stimulation, including increased production of proinflammatory cytokines and myeloid chemokines, neutrophil ROS, and collagen/ECM remodeling pathways. Notably, compared to WT, Lair1 KO infected skin had a similar bacterial burden and neutrophils and monocytes had equivalent S. aureus phagocytosis. These findings support a model in which lack of LAIR1 signaling results in an excessive inflammatory response that does not improve infection control. CTCL tissues harbored similar patterns of increased cytokine and collagen production, suggesting that high levels of LAIR2 in CTCL recapitulates Lair1 KO, causing inflammatory tissue damage and compromising host defense against S. aureus infection.

2024-07-31 | GSE269177 | GEO

LAIR1 prevents excess inflammatory tissue damage in S. aureus skin infection and Cutaneous T-cell Lymphoma [BMDM]

2024-07-31 | GSE269178 | GEO

LAIR1 prevents excess inflammatory tissue damage in S. aureus skin infection and Cutaneous T-cell Lymphoma [BMDM]

Project description:LAIR1 prevents excess inflammatory tissue damage in S. aureus skin infection and Cutaneous T-cell Lymphoma [BMDM]

| PRJNA1120460 | ENA

Neutrophil-derived IL-1β is sufficient for abscess formation in immunity against Staphylococcus aureus in mice

Project description:Neutrophil abscess formation is critical in innate immunity against many pathogens. Here, the mechanism of neutrophil abscess formation was investigated using a mouse model of Staphylococcus aureus cutaneous infection. Gene expression analysis of S. aureus-infected skin revealed that induction of neutrophil recruitment genes was largely dependent upon IL-1beta/IL-1R activation. Unexpectedly, using IL 1beta reporter mice, neutrophils were identified as the primary source of IL-1beta at the site of infection. Furthermore, IL-1beta-producing neutrophils were necessary and sufficient for abscess formation and bacterial clearance. S. aureus-induced IL 1beta production by neutrophils required TLR2, NOD2, FPRs and the ASC/NLRP3 inflammasome. Taken together, IL-1beta and neutrophil abscess formation during an infection are functionally, spatially and temporally linked as a consequence of direct IL-1beta production by neutrophils.

2012-12-05 | GSE36826 | GEO

Neutrophil-derived IL-1β is sufficient for abscess formation in immunity against Staphylococcus aureus in mice

2012-12-05 | E-GEOD-36826 | biostudies-arrayexpress

Blocking LAIR1 signaling in immune cells inhibits tumor development

Project description:LAIR1 is an inhibitory immune cell receptor. We used single cell RNA sequencing (scRNA-seq) to analyze the immune cell distribution in the implanted B16 tumor tissues of Vav-cre human LAIR1 transgenic and LAIR1-/- C57bl/6j mice after control or anti-LAIR1 blocking antibody treatment.

2022-10-27 | GSE212516 | GEO

Homeostatic function of monocyte and interstitial lung macrophages are regulated via collagen binding domain receptor LAIR1 (bulk RNAseq)

Project description:Background: We observed that LAIR1 is highly expressed in murine nonclassical monocytes. This study aims to understand gene expression differences between LAIR1-/- and LAIR1+/+ murine bone marrow nonclassical monocytes. Methods: Ly6C- nonclassical monocytes were sorted out of murine bone marrows and harvested for RNA-seq.

2021-04-12 | GSE171862 | GEO

Homeostatic function of monocyte and interstitial lung macrophages are regulated via collagen binding domain receptor LAIR1 (scRNAseq)

Project description:Monocytes and macrophages play pivotal roles in tissue homeostasis and tumor progression. Here, we show that these cells express high levels of LAIR1, a known receptor for Collagen. Using a high throughput cell-based platform for interactome discovery, we identified Colec12, a protein expressed by stromal cells, as a novel high affinity LAIR1 ligand. Using a combination of genomic, phenotypic, global phosphoproteomics and transcriptomics assays, we corroborated the role of LAIR1 signaling in myeloid cells. Under homeostasis LAIR1 restrained proliferation and promoted survival of non-classical monocytes and dysregulation of this pathway led to an increase in classical monocytes and tissue-infiltrating macrophages in lungs. In tumors, LAIR1 deficiency in myeloid cells exacerbated metastasis to lungs and confirmed LAIR1 as a positive prognostic factor in human metastatic melanoma. Our study shows extracellular matrix provides monocytes and lung interstitial macrophages important homeostatic signals that are mediated via LAIR1. Methods: 10x single cell RNA sequencing was performed to characterize the differences between WT and LAIR1KO lung myeloid cells with and without tumor. Murine lungs were digested, cells were hashtagged and FACS-sorted for Interstitial macrophages, Alveolar macrophages, classical and nonclassical monocytes.

2021-04-12 | GSE171861 | GEO

Spatially-targeted proteomics of S. aureus abscess formation

Project description:Staphylococcus aureus is a major contributor of healthcare-associated infections and able to withstand numerous frequently used antibiotics. In order to develop novel treatment approaches, a deeper understanding of the complex interaction between host and pathogen is required. This is particularly true for the processes during development of tissue abscesses, which are important contributors to acute and persistent staphylococcal infections. Notably, the formation of staphylococcal abscesses takes place in distinct stages. Consequently, studies aiming to elucidate the underlying mechanisms of abscess development have to take temporal and spatial components into account. State-of-the-art proteomic technologies offer insight into complex biological systems. However, the pairing of spatial information and deep proteomic analysis is challenging, complicating the targeted analysis of relatively small-scale and heterogeneous structures like organ abscesses. To overcome existing technical limitations, we have previously introduced the use of a spatially targeted liquid extraction surface analysis (LESA) workflow termed “microLESA”. In our current study, we perform microLESA to investigate the processes at the host-pathogen interface during development of staphylococcal kidney abscesses in a murine model of systemic infection. For this investigation, regions from the abscess community, the interface surrounding the abscess, and the cortex of infected kidneys were extracted and analyzed at both 4- and 10-days post infection. By defining the proteome of different abscess regions across the course of infection, we followed the immune response and bacterial contribution to abscess development through spatial and temporal proteomic changes. The information gathered was then mapped through pathway analysis to characterize the metabolic processes at the host-pathogen interface during staphylococcal infection.

2020-11-30 | PXD019920 | Pride

Exercise prevents fatty liver by modifying the compensatory response of mitochondrial metabolism to excess substrate availability

Project description:Exercise prevents fatty liver by modifying the compensatory response of mitochondrial metabolism to excess substrate availability

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