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The effect of fructose on the inflammatory response of human monocytes

ABSTRACT: The effect of fructose on the inflammatory response of human monocytes

PROVIDER: PRJNA688718 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13332054_1.fastq.gz	Fastqsanger.gz
	SRR13332054_2.fastq.gz	Fastqsanger.gz
	SRR13332055_1.fastq.gz	Fastqsanger.gz
	SRR13332055_2.fastq.gz	Fastqsanger.gz
	SRR13332056_1.fastq.gz	Fastqsanger.gz

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The effect of fructose on the inflammatory response of human monocytes

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The protective effect of inflammatory monocytes during systemic C. albicans infection is dependent on collaboration between C-type lectin-like receptors

Project description:Invasive candidiasis, mainly caused by Candida albicans, is a serious healthcare problem with high mortality rates, particularly in immunocompromised patients. Innate immune cells express pathogen recognition receptors (PRRs) including C-type lectin-like receptors (CLRs) that bind C. albicans to initiate an immune response. Multiple CLRs including Dectin-1, Dectin-2 and Mincle have been proposed individually to contribute to the immune response to C. albicans. However how these receptors collaborate to clear a fungal infection is unknown. Herein, we used novel multi-CLR knockout (KO) mice to decipher the individual, collaborative and collective roles of Dectin-1, Dectin-2 and Mincle during systemic C. albicans infection. These studies revealed an unappreciated and profound role for CLR co-operation in anti-fungal immunity. The protective effect of multiple CLRs was markedly greater than any single receptor, and was mediated through inflammatory monocytes via recognition and phagocytosis of C. albicans, and production of C. albicans-induced cytokines and chemokines. These CLRs were dispensable for mediating similar responses from neutrophils, likely due to lower expression of these CLRs on neutrophils compared to inflammatory monocytes. Concurrent deletion of Dectin-1 and Dectin-2, or all three CLRs, resulted in dramatically increased susceptibility to systemic C. albicans infection compared to mice lacking a single CLR. Multi-CLR KO mice were unable to control fungal growth due to an inadequate early inflammatory monocyte-mediated response. In response to excessive fungal growth, the multi-CLR KO mice mounted a hyper-inflammatory response, likely leading to multiple organ failure. Thus, these data reveal a critical role for CLR co-operation in the effective control of C. albicans and maintenance of organ function during infection.

2019-06-20 | E-MTAB-8030 | biostudies-arrayexpress

Effect of Celecoxib on Perioperative Inflammatory Response in Colon Cancer

Project description:The proposed study aims to investigate how the administration of a drug known to reduce inflammation in humans, Celecoxib, will effect the peri-operative inflammatory response of a patient undergoing primary tumor resection surgery for colon cancer. The proposed project is an exploratory study, and will use data from blood samples and tumor samples to attempt to elucidate the immune and inflammatory response in colon cancer patients undergoing primary resection of their tumors.

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Genome-wide effect of ZBP1-mediated inflammatory response to LPS

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Transcriptome analysis of pulmonary CCR2+ inflammatory monocytes challenged with Cryptococcus neoformans

Project description:The encapsulated yeast Cryptococcus neoformans can cause a fatal meningoencephalitis in immunocompromised patients. C. neoformans infection is acquired through the respiratory tract, but the cellular and molecular mechanisms of the pulmonary innate immune response are still not well defined. To investigate the response of CCR2+ inflammatory monocytes to C. neoformans, we compared the transcriptomes of CCR2+ inflammatory monocytes from the lungs of naïve versus infected mice.

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Triggering of NOD2 receptor converts inflammatory Ly6Chigh into Ly6Clow monocytes with patrolling properties.

Project description:In the present study, we demonstrate that NOD2 receptor triggering by muramyl dipeptide converts blood inflammatory Ly6Chigh monocytes into patrolling Ly6Clow monocytes. Muramyl dipeptide administration to Nr4a1-/- mice, which lack Ly6Clow monocytes, and to Ly6Clow-depleted mice leads to the emergence of blood patrolling monocytes expressing phenotypic profile of typical Ly6Clow monocytes, including high expression of CX3CR1 and LFA1. Furthermore using intravital microscopy in live animal models of inflammatory diseases, we observed that converted Ly6Chigh monocytes are capable of patrolling the endothelium of blood vessels and their presence contributes to reduce the inflammatory response following muramyl dipeptide injection.

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Carotenoids Inhibit Fructose-Induced Inflammatory Response in Human Endothelial Cells and Monocytes.

Project description:ObjectiveThis research is aimed at determining the vascular health characteristics of carotenoids by evaluating their effect on excessive inflammatory response in endothelial and monocyte cells, the main factors of atherosclerosis.MethodsHuman umbilical vein endothelial cells (HUVECs) or U937 monocytes were treated with escalating concentrations (0.1, 0.5, and 1 μM) of five most common carotenoids in human plasma, i.e., α-carotene, β-carotene, β-cryptoxanthin, lutein, and lycopene prior to stimulation with 2 mM fructose. We examined the monocyte adhesion to endothelial cells (ECs) and relevant endothelial adhesion molecules. Chemokine and proinflammatory cytokine production as well as intracellular oxidative stress were also assessed in fructose-stimulated ECs and monocytes.ResultsCarotenoids repressed monocyte adhesion to fructose-stimulated ECs dose dependently via decreasing primarily the expression of endothelial VCAM-1. In ECs and monocytes, three carotenoids, i.e., β-cryptoxanthin, lutein, and lycopene, suppressed the fructose-induced expression of chemokines MCP-1, M-CSF, and CXCL-10 and inflammatory cytokines TNF-α and IL-1β, with CXCL-10 being the most repressed inflammatory mediator. β-Cryptoxanthin, lutein, and lycopene dramatically downregulated the fructose-induced CXCL-10 expression in vascular cells. The reduction in the inflammatory response was associated with a slight but significant decrease of intracellular oxidative stress.ConclusionsOur results show that carotenoids have a variety of anti-inflammatory and antiatherosclerosis activities, which can help prevent or reduce fructose-induced inflammatory vascular diseases.

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Genome-wide analysis of tissue-specific gene expression by Ly6Chi inflammatory monocytes during Toxoplasma gondii infection

Project description:Analysis of Ly6Chi monocytes from small intestine lamina propria (SILP) and blood of day 8 Toxoplasma gondii infected mice at gene expression level. The hypothesis tested in the present study was that Ly6Chi monocytes from SILP have altered expression of regulatory factors to blood monocytes. Results provide important information on the regulatory to effector balance of genes expressed by Ly6Chi monocytes during an acute inflammatory response. Ly6Chi inflammatory monocytes were sorted by FACS from the blood or small intestine lamina propria (SILP) of Toxoplasma gondii infected C57BL/6 mice. Cells were isolated at day 8 after infection and total RNA obtained from sorted populations. Three biological replicates were acquired for both blood and SILP from pooled animals.

2013-05-25 | E-GEOD-46685 | biostudies-arrayexpress

Global genome expression analysis of lamina propria derived WT and Nlrp6-/- Ly6C-hi inflammatory monocytes

Project description:Nlrp6-/- lamina propria Ly6C-hi monocytes in response to AOM/DSS have deficient TNFÎ± production, but increased production of other pro-inflammatory cytokines as compared to WT NLRP6 is a member of the Nod-like receptor family, whose members are involved in the recognition of microbes and/or tissue injury. NLRP6 was previously demonstrated to regulate the production of IL-18 and is important for protecting mice against chemically-induced intestinal injury and colitis-associated colon cancer. However, the cellular mechanisms by which NLRP6 reduces susceptibility to colonic inflammation remain unclear. Here, we determined that NLRP6 expression is specifically upregulated in Ly6Chi inflammatory monocytes that infiltrate into the colon during dextran sulfate sodium (DSS)-induced inflammation. Adoptive transfer of WT Ly6Chi inflammatory monocytes into Nlrp6-/- mice was sufficient to protect them from mortality, significantly reducing intestinal permeability and damage. NLRP6-deficient inflammatory monocytes were specifically defective in TNFÎ± production, which was important for reducing DSS-induced mortality and dependent on autocrine IL-18 signaling by inflammatory monocytes. Our data reveal a previously unappreciated role for NLRP6 in inflammatory monocytes, which are recruited during intestinal injury to promote barrier function and limit bacteria-driven inflammation. This study also highlights the importance of early cytokine responses, particularly NLRP6-dependent and IL-18-dependent TNFÎ± production in preventing chronic dysregulated inflammation. Ly6Chi monocytes were sorted from lamina propria of WT or Nlrp6-/- mice at day 10 of AOM/2%DSS. RNA was extracted and hybridized to the mouse 2.1 ST array.

2016-03-27 | E-GEOD-79631 | biostudies-arrayexpress

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