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Intestinal Epithelial C/EBPβ Deficiency Impairs Colitis-Associated Tumorigenesis by Disrupting CXCL1 /CXCL2/CXCL5-CXCR2-Mediated Neutrophil Infiltration [RNA-seq ]

ABSTRACT: To investigate the function of intestinal-specific cebpb loss in the infiltration of neutrophils, we performed transcriptomic sequencing to compare global gene expression in the colon tissues from AOM/DSS mice models.

ORGANISM(S): Mus musculus

PROVIDER: GSE264497 | GEO | 2025/06/25

REPOSITORIES: GEO

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Intestinal Epithelial C/EBPβ Deficiency Impairs Colitis-Associated Tumorigenesis by Disrupting CXCL1 /CXCL2/CXCL5-CXCR2-Mediated Neutrophil Infiltration [RNA-seq ]

Project description:Intestinal Epithelial C/EBPβ Deficiency Impairs Colitis-Associated Tumorigenesis by Disrupting CXCL1 /CXCL2/CXCL5-CXCR2-Mediated Neutrophil Infiltration [RNA-seq ]

| PRJNA1102849 | ENA

CXCL1-CXCR2 signalling mediates hypertensive retinopathy by inducing macrophage infiltration.

Project description:Inflammation plays an important role in hypertensive retinal vascular injury and subsequent retinopathy. Monocyte chemotaxis via CXCL1-CXCR2 binding has been implicated in various cardiovascular diseases, but the function of CXCL1-CXCR2 signalling involved in retinopathy, which was investigated as angiotensin II (Ang II)-induced retinopathy, is unclear. In our study, we established a hypertensive retinopathy (HR) model by Ang II infusion (3000 ng/min/kg) for 3 weeks. To determine the involvement of CXCR2 signalling, we used CXCR2 knockout (KO) mice or C57BL/6J wild-type (WT) mice as experimental subjects. The mice were treated with a CXCL1 neutralizing antibody or SB225002 (the specific CXCR2 inhibitor). Our results showed that after Ang II treatment, the mRNA levels of CXCL1 and CXCR2 and the number of CXCR2+ inflammatory cells were significantly elevated. Conversely, unlike in the IgG control group, the CXCL1 neutralizing antibody greatly reduced the increase in central retinal thickness induced by Ang II infusion, arteriolar remodelling, superoxide production, and retinal dysfunction in WT mice. Furthermore, Ang II infusion induced arteriolar remodelling, infiltration of Iba1+ macrophages, the production of oxidative stress, and retinal dysfunction, but the symptoms were ameliorated in CXCR2 KO mice and SB225002-treated mice. These protective effects were related to the reduction in the number of CXCR2+ immune cells, particularly macrophages, and the decrease in proinflammatory cytokine (IL-1β, IL-6, TNF-ɑ, and MCP-1) expression in Ang II-treated retinas. Notably, serum CXCL1 levels and the number of CXCR2+ monocytes/neutrophils were higher in HR patients than in healthy controls. In conclusion, this study provides new evidence that the CXCL1-CXCR2 axis plays a vital role in the pathogenesis of hypertensive retinopathy, and selective blockade of CXCL1-CXCR2 activation may be a potential treatment for HR.

| S-EPMC9418605 | biostudies-literature

Staphylococcus aureus Infection Induces the Production of the Neutrophil Chemoattractants CXCL1, CXCL2, CXCL3, CXCL5, CCL3, and CCL7 by Murine Osteoblasts.

Project description:Staphylococcus aureus is the principal causative agent of osteomyelitis, a serious bacterial infection of bone that is associated with progressive inflammatory damage. Bone-forming osteoblasts have increasingly been recognized to play an important role in the initiation and progression of detrimental inflammation at sites of infection and have been demonstrated to release an array of inflammatory mediators and factors that promote osteoclastogenesis and leukocyte recruitment following bacterial challenge. In the present study, we describe elevated bone tissue levels of the potent neutrophil-attracting chemokines CXCL1, CXCL2, CXCL3, CXCL5, CCL3, and CCL7 in a murine model of posttraumatic staphylococcal osteomyelitis. RNA sequencing (RNA-Seq) gene ontology analysis of isolated primary murine osteoblasts showed enrichment in differentially expressed genes involved in cell migration and chemokine receptor binding and chemokine activity following S. aureus infection, and a rapid increase in the expression of mRNA encoding CXCL1, CXCL2, CXCL3, CXCL5, CCL3, and CCL7, in these cells. Importantly, we have confirmed that such upregulated gene expression results in protein production with the demonstration that S. aureus challenge elicits the rapid and robust release of these chemokines by osteoblasts and does so in a bacterial dose-dependent manner. Furthermore, we have confirmed the ability of soluble osteoblast-derived chemokines to elicit the migration of a neutrophil-like cell line. As such, these studies demonstrate the robust production of CXCL1, CXCL2, CXCL3, CXCL5, CCL3, and CCL7 by osteoblasts in response to S. aureus infection, and the release of such neutrophil-attracting chemokines provides an additional mechanism by which osteoblasts could drive the inflammatory bone loss associated with staphylococcal osteomyelitis.

| S-EPMC10112169 | biostudies-literature

mRNAs and miRNAs expression data from AOM/DSS, AOM, DSS and control mouse colon epithelial tissue at day100 when tumor formed in AOM/DSS bearing mice --- miRNA microarray

Project description:To find out which miRNAs are significantly differential expression and potentially involved in the process of inflammation promoting carcinogenesis of colorectal cancer (CRC). We established a colitis-associated CRC (AOM/DSS, Azoxymethane/Dextran sulfate sodium salt) model, colitis (DSS) model and high dose carcinogen (AOM, about 5 times AOM amount given than AOM/DSS model) model. At day 100 when tumor formed in AOM/DSS bearing mice (colitis-associated CRC mice) but no tumor was found in AOM (high dose carcinogen) and DSS model, we employed miRNA microarray as a discovery platform to identify genes with the potential to involve in the progression of CRC promoted by inflammation. 5-7 weeks female BALB/c mice, (1) AOM/DSS group: AOM 12.5mg/kg i.p. at day 1, DSS drinking 5d/21dx3circles from day 5; (2) AOM group: AOM 10mg/kg i.p. 1/weekx6 from day 1; (3) DSS group: DSS drinking 5d/21dx3circles from day 5. The distal colon epithelial tissues were collected at day100 when tumor formed in AOM/DSS bearing mice. The miRNA microarray experiments were performed together.

2013-05-10 | E-GEOD-44983 | biostudies-arrayexpress

mRNAs and miRNAs expression data from AOM/DSS, AOM, DSS and control mouse colon epithelial tissue at day100 when tumor formed in AOM/DSS bearing mice --- mRNA expression data

Project description:To find out which mRNAs are significantly differential expression and potentially involved in the process of inflammation promoting carcinogenesis of colorectal cancer (CRC). We established a colitis-associated CRC (AOM/DSS, Azoxymethane/Dextran sulfate sodium salt) model, colitis (DSS) model and high dose carcinogen (AOM, about 5 times AOM amount given than AOM/DSS model) model. At day 100 when tumor formed in AOM/DSS bearing mice (colitis-associated CRC mice) but no tumor was found in AOM (high dose carcinogen) and DSS model, we employed whole genome microarray expression profiling as a discovery platform to identify genes with the potential to involve in the progression of CRC promoted by inflammation. 5-7 weeks female BALB/c mice, (1) AOM/DSS group: AOM 12.5mg/kg i.p. at day 1, DSS drinking 5d/21dx3circles from day 5; (2) AOM group: AOM 10mg/kg i.p. 1/weekx6 from day 1; (3) DSS group: DSS drinking 5d/21dx3circles from day 5. The distal colon epithelial tissues were collected at day100 when tumor formed in AOM/DSS bearing mice. The whole genome microarray expression profiling experiments were performed together.

2013-05-10 | E-GEOD-44904 | biostudies-arrayexpress

The MicroRNAmiR-223constrains Colitis-associated tumorigenesis by limiting myeloid cell infiltration and Chemokine expression

Project description:Aberrant intestinal inflammation plays a critical role in the development of colitis-associated colorectal cancer (CAC), yet the mechanisms behind this progression are not clearly defined. While altered microRNA (miRNA) expression is observed in CAC, it is unclear how myeloid-specific microRNA’s impact on the inflammatory process that underpins the continuum from Ulcerative colitis (UC) to tumorigenesis. Here we used the Azoxymethane-Dextran Sodium Sulfate (AOM-DSS) (10mg/kg) model of CAC on miR-223-/y and WT mice, with an overall aim of identifying differences in their expression profiles following AOM/DSS treatment.

2024-10-01 | GSE245724 | GEO

mRNAs and miRNAs expression data from AOM/DSS, AOM, DSS and control mouse colon epithelial tissue at day100 when tumor formed in AOM/DSS bearing mice --- miRNA microarray

2013-05-10 | GSE44983 | GEO

mRNAs and miRNAs expression data from AOM/DSS, AOM, DSS and control mouse colon epithelial tissue at day100 when tumor formed in AOM/DSS bearing mice --- mRNA expression data

2013-05-10 | GSE44904 | GEO

Chemokine Cxcl1-Cxcl2 heterodimer is a potent neutrophil chemoattractant.

Project description:Microbial infection is characterized by release of multiple proinflammatory chemokines that direct neutrophils to the insult site. How collective function of these chemokines orchestrates neutrophil recruitment is not known. Here, we characterized the role for heterodimer and show that the Cxcl1-Cxcl2 heterodimer is a potent neutrophil chemoattractant in mice and can recruit more neutrophils than the individual chemokines. Chemokine-mediated neutrophil recruitment is determined by Cxcr2 receptor signaling, Cxcr2 endocytosis, and binding to glycosaminoglycans. We have now determined heterodimer's Cxcr2 activity using cellular assays and Cxcr2 density in blood and recruited neutrophils in heterodimer-treated mice. We have shown that the heterodimer binds glycosaminoglycans with higher affinity and more efficiently than Cxcl1 or Cxcl2. These data collectively indicate that optimal glycosaminoglycan interactions and dampened receptor activity acting in concert in a dynamic fashion promote heterodimer-mediated robust neutrophil recruitment. We propose that this could play a critical role in combating infection.

| S-EPMC10673714 | biostudies-literature

Staphylococcus aureus infection induces the production of the neutrophil chemoattractants CXCL1, CXCL2, CXCL3, CXCL5, CCL3, and CCL7 by osteoblasts

Project description:Staphylococcus aureus is the principal causative agent of osteomyelitis, a serious bacterial infection of bone that is associated with progressive inflammatory damage. Bone-forming osteoblasts have increasingly been recognized to play an important role in the initiation and progression of detrimental inflammation at sites of infection, and have been demonstrated to release an array of inflammatory mediators and factors that promote osteoclastogenesis and leukocyte recruitment following bacterial challenge. In the present study, we describe elevated bone tissue levels of the potent neutrophil-attracting chemokines, CXCL1, CXCL2, CXCL3, CXCL5, CCL3, and CCL7, in a murine model of post-traumatic staphylococcal osteomyelitis. RNA-Seq gene ontology analysis of isolated primary murine osteoblasts showed enrichment in differentially expressed genes involved in cell migration and chemokine receptor binding and chemokine activity following S. aureus infection, and a rapid increase in the expression of mRNA encoding CXCL1, CXCL2, CXCL3, CXCL5, CCL3, and CCL7, in these cells. Importantly, we have confirmed that such upregulated gene expression results in protein production with the demonstration that S. aureus challenge elicits the rapid and robust release of these chemokines by osteoblasts and does so in a bacterial dose-dependent manner. Furthermore, we have confirmed the ability of soluble osteoblast-derived chemoattractants to elicit the migration of a neutrophil-like cell line. As such, these studies demonstrate the robust production of CXCL1, CXCL2, CXCL3, CXCL5, CCL3, and CCL7, by osteoblasts in response to S. aureus infection, and the release of such neutrophil-attracting chemokines provides an additional mechanism by which osteoblasts could drive the inflammatory bone loss associated with staphylococcal osteomyelitis.

2022-11-12 | GSE217455 | GEO

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