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Fecal metagenome dataset of patients with gouty arthritis

ABSTRACT: Multi-kingdom characterization of the gut microbiota in patients with gouty arthritis

PROVIDER: PRJEB58696 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR11599978_1.fastq.gz	Fastqsanger.gz
	ERR11599978_2.fastq.gz	Fastqsanger.gz
	ERR11605808_1.fastq.gz	Fastqsanger.gz
	ERR11605808_2.fastq.gz	Fastqsanger.gz
	ERR11634315_1.fastq.gz	Fastqsanger.gz

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Multimodal smart systems reprMultimodal smart systems reprogram macrophages and remove urate to treat gouty arthritisogram macrophages and remove urate to treat gouty arthritis

Project description:Gouty arthritis (GA) is a chronic and progressive disease that often develops due to high urate levels, leading to joint damage and characterized by an inflammatory immune microenvironment (IIMe). Quantitative proteomics further revealed D-N camouflaged with hybid membranes of M2 exosome and its parent microphage (D-N[EM2]) treated GA disease mechanisms.

2024-07-02 | PXD051823 | Pride

Lymphatic vessels drain monosodium urate and activate immunity in gouty arthritis

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Lymphatic vessels drain monosodium urate and activate immunity in gouty arthritis

Project description:Gouty Arthritis (GA) is caused by urate deposition in the joint capsule, cartilage, bone, and surrounding tissues to trigger recurrent attacks of acute joint inflammation. However, the clearance mechanism of urate deposition is still not clear. We aimed to investigate whether lymphatics vessels can drain monosodium and involve in the immune process of GA. Methods: Inguinal lymph nodes (LNs) in 4 normal volunteers and 4 patients with acute flare of GA were examined by ultrasound. Acute and chronic GA flare mouse models were established by intra-footpad administrations of monosodium urate (MSU) for 1 week or 1 month. Mice were treated with VEGFR-3 inhibitor or undergone popliteal lymph node (PLN) excision or PLN macrophage depletion. The severity of foot inflammation, lymphatic draining function, concentration of uric acid (UA), and macrophage population were examined. Macrophages were co-cultured with MSU-treated lymphatic endothelial cells (LECs) and differential gene expression of LECs was assessed by Agilent gene expression microarray. Results: 1) Draining LNs were enlarged in patients with GA flare and GA mouse models. 2) The lymphatic function and structure were abnormal in GA mouse models. 3) Acute GA mice had elevated UA levels in draining LNs, but not in the serum, while chronic GA mice had elevated UA levels in both LNs and serum. 4) Blockade of VEGFR-3 reduced foot inflammation in chronic GA mice. 5) MSU induces pro-inflammatory polarization of macrophages by inducing LEC inflammation. 6) PLN local depletion of macrophages or removal of PLNs alleviated foot inflammation in GA. Conclusions: Lymphatics drain MSU to the draining LNs to clear deposited urate in the distal extremity and induce LECs to stimulate macrophage pro-inflammatory response during GA. We have identified a novel mechanism about MSU clearance and pro-inflammatory macrophage activation, and provided possible therapeutic approach for GA.

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The NADase CD38 is a central regulator in gouty inflammation and a novel druggable therapeutic target

Project description:Objectives: In gout, flares of severely painful inflammatory arthritis intersect with metabolism, circadian rhythm, and macrophage activation. NAD+ is a necessary cofactor and key metabolite in cellular bioenergy homeostasis, and NAD+ suppresses the NLRP3 inflammasome and inflammation. However, cellular NAD+ declines in inflammatory states, associated with increased activity of the leukocyte-expressed NADase CD38. Gouty arthritis is principally prevented and treated with nonselective and frequently toxic drugs (colchicine, NSAIDs, corticosteroids). Hence, we tested the potential role of therapeutically targeting CD38 and NAD+ in gout. Methods: We studied cultured mouse wild type and CD38 knockout (KO) murine bone marrow derived macrophages (BMDMs) stimulated by monosodium urate (MSU) crystals, and the air pouch gout synovitis model. Results: MSU crystals induced CD38 in BMDMs in vitro, associated with NAD+ depletion, and IL-1b and CXCL1 release, effects reversed by pharmacologic CD38 inhibitors (apigenin, 78c). Mouse air pouch inflammatory responses to MSU crystals were blunted by CD38 KO and apigenin. Pharmacologic CD38 inhibition suppressed MSU crystal-induced NLRP3 inflammasome activation and increased anti-inflammatory SIRT3-SOD2 in macrophages. BMDM RNA-seq analysis of 176 differentially expressed genes (DEGs) revealed CD38 control of multiple MSU crystal-modulated inflammation pathways. The top DEGs included the circadian rhythm modulator GRP176, and the metalloreductase STEAP4 that mediates iron homeostasis, and promotes oxidative stress and NF-kB activation when it is overexpressed. Conclusion: CD38 and NAD+ depletion are druggable targets controlling the MSU crystal- induced inflammation program. Targeting CD38 and NAD+ are potentially novel selective molecular approaches to limit gouty arthritis.

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Nuclear Receptor Coactivator 6 is a Critical Regulator of NLRP3 Inflammasome Activation and Gouty Arthritis

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Expression profiling of ankle joint of a mouse model of gouty arthritis uncovers potential mechanisms involved in pain and inflammation

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