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Murine gut microbiota dysbiosis via enteric infection modulates the foreign body response to a distal biomaterial implant

ABSTRACT: Murine gut microbiota dysbiosis via enteric infection modulates the foreign body response to a distal biomaterial implant

PROVIDER: PRJNA1245270 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32945544_1.fastq.gz	Fastqsanger.gz
	SRR32945544_2.fastq.gz	Fastqsanger.gz
	SRR32945545_1.fastq.gz	Fastqsanger.gz
	SRR32945545_2.fastq.gz	Fastqsanger.gz
	SRR32945546_1.fastq.gz	Fastqsanger.gz

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Murine gut microbiota dysbiosis via enteric infection modulates the foreign body response to a distal biomaterial implant

Project description:The gut microbiota influences systemic immunity and the function of distal tissues, including the brain, liver, skin, lung, and muscle. However, the role of the gut microbiota in the foreign body response (FBR) and fibrosis is largely unexplored. To investigate this connection, we perturbed the homeostasis of the murine gut microbiota via infection with the pathogenic bacterial species enterotoxigenic Bacteroides fragilis (ETBF) and implanted particulate material (mean particle size <600 μm) of the synthetic polymer polycaprolactone (PCL) into a distal muscle injury. ETBF infection in mice led to increased neutrophil and γδ T cell infiltration into the PCL implant site. ETBF infection alone promoted systemic inflammation, increased levels of neutrophils in lymphoid tissues, and altered skeletal muscle gene expression. At the PCL implant site, we found significant changes in the transcriptome of sorted stromal cells between infected and control mice, including differences related to ECM components such as proteoglycans and glycosaminoglycans. However, we did not observe ETBF-induced differences in fibrosis levels. These results demonstrate the ability of the gut microbiota to mediate long-distance effects such as immune and stromal responses to a distal biomaterial implant.

2025-04-30 | GSE293564 | GEO

Allometric tissue-scale forces activate mechanoresponsive immune cells to determine pathological foreign body response to biomedical implants

Project description:Allometric tissue-scale forces at the implant-tissue interface drive pathological foreign body response.

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Engineered biomaterial immunological niches as a surrogate for diseased tissue in chronic progressive EAE

Project description:We use a subcutaneous biomaterial implant as a surrogate for sampling immune cells phenotypes in murine chronic EAE. These implants are microporous polycaprolactone scaffolds that form immunological niches that get vascularized and capture both innate and adaptive immune cells. These niches can be minimally invasively biopsied, allowing for multiple samples to be collected from the same mouse at various timepoints in disease: presymptomatic (Day 7) and early state disease (Day 9). This study investigates immune dynamics over time in subclinical and early stage chronic progressive EAE at a distal biomaterial-based immunological niche.

2025-01-24 | GSE287968 | GEO

Role of Macrophages in the Foreign Body Response to Poly(ethylene glycol) Hydrogels

Project description:Macrophages are known to be the drivers of the Foreign Body Response (FBR) to implanted biomaterials. While each macrophage population may polarize into distinct phenotypes, the timescales of this process and their functional roles in the FBR are not known. The goal of this study was to investigate temporal changes in macrophage polarization over the course of the FBR to a PEG hydrogel implant. RNA-seq methods were applied to map temporal changes in the transcriptome of implant-associated monocytes, which represent newly arrived blood monocytes prior to their maturation into macrophages, and separately implant-associated macrophages, which represent both recruited and tissue resident macrophages. The transcriptomics analysis of implant-associated monocytes revealed that pro-inflammatory pathways were up-regulated early and continued to increase at day 14, but by day 28 began to subside. On the contrary, macrophages were initially in a pro-inflammatory state, but underwent a shift in their polarization state to an alternatively activated pro-fibrotic state by day 14, correlating with the emergence of the fibrous capsule. They retained this state through day 28, which correlated with the continued growth of the fibrous capsule around the hydrogel implant.

2022-01-03 | GSE185761 | GEO

Single-cell Analysis of Surface Topography-induced Foreign Body Response to Silicone Implants

Project description:Silicone-based medical devices are widely used in chronic implants and are generally perceived to be safe. However, immune-related complications including malignancies have recently been linked to textured breast implants. Here, we examine the influence of clinically approved breast implants surface features on host immune responses. Prosthetics with surface roughness of 0, 4, and 90 (Ra) were implanted in mammary fat pads of mice for 2 weeks and cells adjacent to the resulting tissue capsules were evaluated for foreign body immune responses using single-cell RNA-seq. Our findings identify a unique and finely tuned surface topography that is capable of modulating implant immunity to suppress foreign body response.

2021-05-28 | GSE164645 | GEO

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Project description:Peri-implant fibrosis is one of the most common reasons for implant failure and surgical revision after prosthetic joint replacement. This type of surgical revisionis associated with substantial additional morbidity and healthcare costs. However, the cellular and molecular mediators of peri-implant fibrosis remain unclear. Here, we show that peri-implant fibrotic tissue in mice and humans is largely composed of a specific population of leptin receptor-expressing(LEPR+) cells and that these LEPR+cells are necessary and sufficient to both generate and maintain peri-implant fibrotic tissue. Genetic ablation of LEPR+cells prevents peri-implant fibrosis, and implantation of LEPR+cells from peri-implant fibrotic tissue is sufficient to induce fibrosis in secondary hosts. We further identify adhesion G protein-coupled receptorF5 (ADGRF5) as a crucial mediator of the fibrotic response by LEPR+cells, as conditional deletion of ADGRF5 in LEPR+cells attenuates peri-implant fibrosis while augmenting peri-implant bone formation. Finally, we demonstrate that inhibition of ADGRF5 by intra articular or systemic administration of neutralizing anti-ADGRF5prevents and reverses peri-implant fibrosis. Thus, pharmaceutical agents that inhibit the ADGRF5 pathway inLEPR+cells may represent a new approach to prevent and treat peri-implant fibrosis.

2024-03-10 | GSE227128 | GEO

Transcriptomic profile of Lin negative, LEPR positive cells of murine peri-implant fibrous tissue and peri-implant bone

Project description:To investigate the transcriptomic profile difference between LEPR cells in peri-implant fibrous tissue and peri-implant bone

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Comparison of the gene expression of periimplantitis affected peri-implant tissue and healthy peri-implant tissue in vivo in human.

Project description:In this study we want to ascertain the differences and similarities of infected and inflammated peri implant tissue versus healthy peri implant tissue at the mRNA level.

2014-05-14 | GSE57631 | GEO

Inflammasome components ASC and AIM2 modulate the acute phase of biomaterial implant-induced foreign body responses.

Project description:Detailing the inflammatory mechanisms of biomaterial-implant induced foreign body responses (FBR) has implications for revealing targetable pathways that may reduce leukocyte activation and fibrotic encapsulation of the implant. We have adapted a model of poly(methylmethacrylate) (PMMA) bead injection to perform an assessment of the mechanistic role of the ASC-dependent inflammasome in this process. We first demonstrate that ASC(-/-) mice subjected to PMMA bead injections had reduced cell infiltration and altered collagen deposition, suggesting a role for the inflammasome in the FBR. We next investigated the NLRP3 and AIM2 sensors because of their known contributions in recognising damaged and apoptotic cells. We found that NLRP3 was dispensable for the fibrotic encapsulation; however AIM2 expression influenced leukocyte infiltration and controlled collagen deposition, suggesting a previously unexplored link between AIM2 and biomaterial-induced FBR.

| S-EPMC4748295 | biostudies-literature

Comparison of Gene Expression between Peri-implant Soft Tissue and Oral Mucosal Tissue

Project description:The mucosal penetration area formed by implant placement is critical problems of dental implant treatment, because epithelial barrier is broken and it can become a source of inflammation. To clarify the influence and risk caused by dental implant treatment in peri-implant soft tissue, we compared to gene expression profile of peri-implant soft tissue and oral mucosal tissue with microarray analysis.

2013-01-24 | GSE43744 | GEO

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