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Temporal programming of T-helper 17 (TH17) cell differentiation by SAA1+IL6 measured by RNA-Seq

ABSTRACT: We report that the Serum Amyloid A protein, SAA1, is a novel, soluble co-factor able to promote pathogenic TH17 differentiation.

ORGANISM(S): Mus musculus

PROVIDER: GSE132761 | GEO | 2019/12/05

REPOSITORIES: GEO

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Temporal programming of T-helper 17 (TH17) cell differentiation by SAA1+IL6 measured by RNA-Seq

Project description:Temporal programming of T-helper 17 (TH17) cell differentiation by SAA1+IL6 measured by RNA-Seq

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Effect of serum amyloid A1 (SAA1) on gene expression in primary murine macrophages

Project description:Macrophages are important regulators of the immune system and are critically involved in the pathophysiology of many diseases. Serum amlyoidosis is a protein misfolding disease which can follow chronic inflammatory conditions. Deposition of fibrils formed from serum amyloid A1 (SAA1) protein occurs systemically and can lead to severe or even fatal outcomes. Macrophages play a critical role in the misfolding and deposition of SAA1-derived fibrils and the role of macrophages in this context has been studied extensively. It is known that SAA1 can bind to some surface receptors on macrophages and it is taken up by the macrophages and metabolized in the lysosomes. On the other hand, the effect of SAA1 on macrophage physiology has been much less investigated so far. Therefore, we aim to investigate the effect of SAA1 on macrophage gene expression by gene microarray analysis. To this end, primary peritoneal macrophages from NMRI mice were treated with endotoxin-free recombinantly expressed full-length mSAA1 for 6 and 24 h and gene expression was analyzed.

2021-07-20 | GSE155278 | GEO

SAA1-dependent reprogramming of adipocytes by tumor cells is associated with triple negative breast cancer aggressiveness

Project description:Cancer development and progression depend on tumor cell intrinsic factors, the tumor microenvironment and host characteristics. Despite the identification of the plasticity of adipocytes, the primary breast stromal cells, both in physiology and cancer, we lack a complete understanding of mechanisms that regulate adipocyte-tumor cell crosstalk. Here we dissected the breast cancer crosstalk with adipocytes and studied relevant molecules. We identified that the ability of breast cancer cells to dedifferentiate adipocytes is intrinsic subtype-dependent, with all breast cancer subtypes, except for HER2+ER+ subtype, capable of inducing this phenomenon. Crosstalk between breast cancer cells and adipocytes in vitro increased cancer stem-like features and recruitment of pro-tumorigenic immune cells, through chemokine production. Serum amyloid A1 (SAA1) was in vitro identified as a regulator of the adipocyte dedifferentiation program in triple-negative breast cancer (TNBC) through CD36 and P2XR7 signaling. In human TNBCs, SAA1 expression was associated with CAA infiltration, inflammation, stimulated lipolysis, stem-like properties and distinct tumor immune microenvironment. Our findings provide evidence that interaction between tumor cells and adipocytes through SAA1 release is relevant to the aggressiveness of TNBC, potentially supporting its targeting.

2024-01-15 | PXD041186 | Pride

Integrated analysis Of Biopsies From Inflammatory Bowel Disease Patients Identifies SAA1 As A Link Between Mucosal Microbes With TH17 And TH22 Cells [diseased subjects]

Project description:Inflammatory bowel diseases (IBD) are believed to be driven by dysregulated interactions between the host and the gut microbiota. Our goal is to characterize the relationships between mucosal T cells, the host tissue environment and microbial communities in IBD patients to identify new therapeutic targets. We identified 26 predictors from our combined data set that were effective in distinguishing between regions of the intestine undergoing active inflammation and regions that were normal. Network analysis on these 26 predictors revealed SAA1 as the most connected node linking the abundance of the genus Bacteroides with the production of IL17 and IL22 by CD4+ T cells. The SAA1-linked microbial and transcriptome interactions were further validated with data from the pediatric IBD RISK cohort. This study identifies expression of SAA1 as an important link between mucosal T cells, microbial communities and their tissue environment in IBD patients. A combination of FACS, gene expression and microbial profiling can distinguish between intestinal inflammatory states in IBD regardless of disease types.

2017-11-11 | GSE96665 | GEO

Effect of serum amyloid A1 (SAA1) on gene expression in primary murine macrophages

Project description:Effect of serum amyloid A1 (SAA1) on gene expression in primary murine macrophages

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N-acetylglucosamine inhibits T-helper 1 (Th1)/T-helper 17 (Th17) cell responses and treats experimental autoimmune encephalomyelitis.

Project description:Current treatments and emerging oral therapies for multiple sclerosis (MS) are limited by effectiveness, cost, and/or toxicity. Genetic and environmental factors that alter the branching of Asn (N)-linked glycans result in T cell hyperactivity, promote spontaneous inflammatory demyelination and neurodegeneration in mice, and converge to regulate the risk of MS. The sugar N-acetylglucosamine (GlcNAc) enhances N-glycan branching and inhibits T cell activity and adoptive transfer experimental autoimmune encephalomyelitis (EAE). Here, we report that oral GlcNAc inhibits T-helper 1 (Th1) and T-helper 17 (Th17) responses and attenuates the clinical severity of myelin oligodendrocyte glycoprotein (MOG)-induced EAE when administered after disease onset. Oral GlcNAc increased expression of branched N-glycans in T cells in vivo as shown by high pH anion exchange chromatography, MALDI-TOF mass spectroscopy and FACS analysis with the plant lectin l-phytohemagglutinin. Initiating oral GlcNAc treatment on the second day of clinical disease inhibited MOG-induced EAE as well as secretion of interferon-?, tumor necrosis factor-?, interleukin-17, and interleukin-22. In the more severe 2D2 T cell receptor transgenic EAE model, oral GlcNAc initiated after disease onset also inhibits clinical disease, except for those with rapid lethal progression. These data suggest that oral GlcNAc may provide an inexpensive and nontoxic oral therapeutic agent for MS that directly targets an underlying molecular mechanism causal of disease.

| S-EPMC3220534 | biostudies-literature

Effect of HDL enriched with Serum Amyloid A1 (HDL+SAA1) on Gene Expression by Classical CD14+/CD16- Human Peripheral Blood Monocytes from Asthmatics

Project description:IL-6 and PTGS2 were the most highly expressed mRNA transcripts in Classical CD14+/CD16- Monocytes from Asthmatic Subjects in response to treatment with HDL+SAA1

2020-07-31 | GSE134591 | GEO

An IL-23R/IL-22 circuit regulates epithelial serum amyloid A to promote local effector Th17 responses II [RNA-Seq]

Project description:Purpose: The goals of this study are to compare in vitro polarized T helper 17 cell transcriptome profiling (RNA-seq) in the presence or absence of recombinant murine SAA1 Methods: Th17 mRNA profiles of 96hrs in vitro cultured T helper 17 cells treated with vehicle or recombinant murine SAA1 were generated by deep sequencing, using Illumina RapidRun. The sequence reads that passed quality filters were analyzed at the transcript isoform level with two methods: Burrows–Wheeler Aligner (BWA) and TopHat followed by CuffDiff. qRT–PCR validation was performed using SYBR Green assays. Results: 177 genes were changed more than 2 folds in the presence of recombinant murine SAA1. Conclusions: Our study suggest that SAA1 could augment subset of Th17 transcription program in vitro.

2015-10-09 | GSE71281 | GEO

Inflammation-induced acute phase response in skeletal muscle and critical illness myopathy

Project description:Objectives: Systemic inflammation is a major risk factor for critical-illness myopathy (CIM) but its pathogenic role in muscle is uncertain. We observed that interleukin 6 (IL-6) and serum amyloid A1 (SAA1) expression was upregulated in muscle of critically ill patients. To test the relevance of these responses we assessed inflammation and acute-phase response at early and late time points in muscle of patients at risk for CIM. Design: Prospective observational clinical study and prospective animal trial. Setting: Two intensive care units (ICU) and research laboratory. Patients/Subjects: 33 patients with Sequential Organ Failure Assessment scores ≥8 on 3 consecutive days within 5 days in ICU were investigated. A subgroup analysis of 12 patients with, and 18 patients without CIM (non-CIM) was performed. Two consecutive biopsies from vastus lateralis were obtained at median days 5 and 15, early and late time points. Controls were 5 healthy subjects undergoing elective orthopedic surgery. A septic mouse model and cultured myoblasts were used for mechanistic analyses. Measurements and Main Results: Early SAA1 expression was significantly higher in skeletal muscle of CIM compared to non-CIM patients. Immunohistochemistry showed SAA1 accumulations in CIM patients at the early time point, which resolved later. SAA1 expression was induced by IL-6 and tumor necrosis factor-alpha in human and mouse myocytes in vitro. Inflammation-induced muscular SAA1 accumulation could be reproduced in a sepsis mouse model. Conclusions: Skeletal muscle contributes to general inflammation and acute-phase response in CIM patients. Muscular SAA1 could be important for CIM pathogenesis. Trial registration: ISRCTN77569430. Expression analysis of patients with and without CIM (non-CIM) was performed. Date were quantile normalized using Partek Genomic Suite 6.5, RMA background correction, pre background adjustment for GC content and data were limited to the full dataset

2014-05-06 | E-GEOD-53702 | biostudies-arrayexpress

RNA-seq of wild type and GLUT3-deficient T helper 17 (Th17) cells

Project description:RNA-sequencing and analysis of in vitro differentiated Th1 and Th17 cells isolated from WT and Slc2a3-fl/fl Cd4-cre mice.

2022-02-13 | GSE192659 | GEO