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Whole Genome microarray analysis BMDMs from cmo (Pstpip2 functional knockout), cmo IL1R+/-, and cmo IL-1R-/- mice.

ABSTRACT: Because the cmo mouse (model of human CRMO) is protected from disease on an IL1R-/- background, a gene expression microarray experiment was performed to determine which genes are potentially involved in the pathogenesis of disease in the context of the absence of IL1R activity. RNA was extracted from cultured bone marrow-derived macrophages from the three mouse strains and analyzed for differential gene expression.

ORGANISM(S): Mus musculus

PROVIDER: GSE94112 | GEO | 2017/03/01

SECONDARY ACCESSION(S): PRJNA368956

REPOSITORIES: GEO

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Mus musculus

Project description:Whole Genome microarray analysis BMDMs from cmo (Pstpip2 functional knockout), cmo IL1R+/-, and cmo IL-1R-/- mice.

| PRJNA368956 | ENA

Chronic inflammation decreases HSC fitness via hyperactivation of the druggable IL-6/Jak/Stat3 signaling pathway.

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IL-1/IL-1R Signaling in Head and Neck Cancer.

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Cop1 wildtype and knockout ATAC-seq in BMDMs

Project description:The realization in the last decade that dysregulated microglia are intimately involved in Alzheimer’s disease (AD) pathogenesis has been a major advance. The precise mechanisms controlling pathogenic programs of microglia gene expression, however, remain poorly understood. The transcription factor (TF) c/EBPß is highly expressed in microglia and is known to regulate expression of pro-inflammatory genes. Notably, c/EBPß is upregulated in AD. Despite mounting evidence that the levels of this pivotal pro-inflammatory TF are tightly regulated, how this is achieved is unclear as alterations in its amounts are not reflected in transcript levels. Remarkably, we find that this TF is primarily regulated post-translationally. Here we show that the ubiquitin ligase Cop1 functions as a “brake” on microglial activation by targeting c/EBPß for ubiquitination and subsequent proteasomal mediated degradation. In the absence of Cop1, c/EBPß protein rapidly and dramatically accumulates leading to engagement of a potent pro-inflammatory and ApoE gene-expression program, evidenced by increased neurotoxicity in microglia-neuronal co-cultures. Antibody blocking studies revealed that the neurotoxicity was almost entirely attributable to complement. Unexpectedly, loss of a single allele of c/EBPß, rescued the pro-inflammatory phenotype underscoring a significant gene dosage effect. We also found that Cop1 deletion accelerated disease progression in a mouse model of tau-mediated neurodegeneration where elevated ApoE plays a deleterious role. Taken together these results point to c/EBPß as a potential therapeutic target for inflammation-driven neurodegeneration as the heterozygote animal is otherwise normal.

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RNA Sequencing Analysis of BMDMs from Wild Type and DRD5-/- mice

Project description:We identified that DRD5 protected against DDS-induced colitis, and DRD5 deficiency in macrophages promoted the development of DSS-induced colitis.The purpose of this experiment was to identify how DRD5 protected against DSS-induced colitis.

2021-05-26 | GSE159206 | GEO

Targeting TLR/IL-1R signalling in human diseases.

Project description:The members of Toll-like receptor/interleukin (IL)-1 receptor (TLR/IL-1R) superfamily play a fundamental role in the immune response. These receptors detect microbial components and trigger complex signalling pathways that result in increased expression of multiple inflammatory genes. On the other hand, an aberrant activation of TLR/IL-1R signalling can promote the onset of inflammatory and autoimmune diseases, raising the interest in the development of therapeutic strategies for the control of their function. In this review, we illustrate the structural and functional features of TLR/IL-1R proteins and discuss some recent advances in the approaches undertaken to develop anti-inflammatory therapeutic drugs. In particular, we will focus on inhibitors, such as decoy peptides and synthetic mimetics, that interfere with protein-protein interactions between signalling molecules of the TLR/IL-1R superfamily. Given their central role in innate and adaptive immune responses, it is foreseen that pharmaceutical modulation of TLR/IL-1R signalling pathways by these drugs might yield clinical benefits in the treatment of inflammatory and autoimmune diseases.

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The toll interleukin-1 receptor (IL-1R) 8/single Ig domain IL-1R-related molecule modulates the renal response to bacterial infection.

Project description:Our immune system has to constantly strike a balance between activation and inhibition of an inflammatory response to combat invading pathogens and avoid inflammation-induced collateral tissue damage. Toll interleukin-1 receptor 8 (IL-1R-8)/single Ig domain IL-1R-related molecule (TIR8/SIGIRR) is an inhibitor of Toll-like receptor (TLR)/IL-1R signaling, which is predominantly expressed in the kidney. The biological role of renal TIR8 during infection is, however, unknown. We therefore evaluated renal TIR8 expression during Escherichia coli pyelonephritis and explored its role in host defense using TIR8(-/-) versus TIR8(+/+) mice. We found that TIR8 protein is abundantly present in the majority of cortical tubular epithelial cells. Pyelonephritis resulted in a significant downregulation of TIR8 mRNA in kidneys of TIR8(+/+) mice. TIR8 inhibited an effective host response against E. coli, as indicated by diminished renal bacterial outgrowth and dysfunction in TIR8(-/-) mice. This correlated with increased amounts of circulating and intrarenal neutrophils at the early phase of infection. TIR8(-/-) tubular epithelial cells had increased cytokine/chemokine production when stimulated with lipopolysaccharide (LPS) or heat-killed E. coli, suggesting that TIR8 played an anti-inflammatory role during pathogen stimulation by inhibiting LPS signaling. These data suggest that TIR8 is an important negative regulator of an LPS-mediated inflammatory response in tubular epithelial cells and dampens an effective antibacterial host response during pyelonephritis caused by uropathogenic E. coli.

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Correlation of nuclear pIGF-1R/IGF-1R and YAP/TAZ in a tissue microarray with outcomes in osteosarcoma patients.

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