Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA103009 | ENA |
REPOSITORIES: ENA
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Project description:Leukotriene B4 (LTB4) is a potent lipid mediator of inflammation, implicated in numerous diseases including atherosclerosis. We have used primary human monocytes, which express both receptors, to analyze transcriptional responses to LTB4. Comparisons were made between LTB4- and vehicle-treated samples at the same time point. The analysis showed that expression of 72 genes was upregulated at least two-fold at two time points. These genes include multiple chemokines as well as some genes with unknown function. Keywords: time course
2007-10-18 | GSE9332 | GEO
Project description:Gliotoxin (GT), a major secondary metabolite and virulence factor of Aspergillus fumigatus, suppresses innate immunity and supports the evasion of host immune responses. Recently, we revealed that GT blocks leukotriene (LT)B4 formation by directly inhibiting LTA4 hydrolase (LTA4H) in activated human neutrophils and monocytes. Here, we elucidated the impact of GT on LTB4 biosynthesis and the complex lipid mediator network in human M1- and M2-like monocyte-derived macrophage (MDM) subtypes and studied the respective consequences for innate immune cell functions. Notably, in resting MDMs, GT elicited prostaglandin and 12/15-lipoxygenase product formation, although less efficient than bacterial exotoxins. In activated MDM, LTB4 formation was effectively suppressed by GT, connected to impaired macrophage phagocytic activity, and detrimental consequences for neutrophil movement and migration. Conclusively, GT impairs functions of activated innate immune cells through suppression of LTB4 formation, while GT may prime the immune system by provoking prostaglandin formation and 12/15-lipoxygenase-derived LM.
2024-11-13 | PXD045819 | Pride
Project description:total RNA from mouse (male c57BL/6) spleen labeled with Cy3 vs total RNA from mouse (male c57BL/6) B cells treated with Leukotriene B4 (LTB4) labeled with Cy5- time course with repeats Keywords: ordered
2003-04-14 | GSE390 | GEO
Project description:In this model, naïve blood neutrophils are migrated through a small airway epithelium grown at air-liquid interface toward CF airway fluid supernatant (CFASN, which corresponds to sputum sequentially centrifuged to remove cells and bacteria) or leukotriene B4 (LTB4, transmigration control), placed apically.
2021-02-19 | GSE167069 | GEO
Project description:Nonalcoholic steatohepatitis (NASH) is a prevalent disease that can ultimately progress to more severe forms of disease including liver fibrosis, cirrhosis, hepatocellular carcinoma (HCC), and ultimately death. A key feature of NASH is lobular inflammation, which is a major driver of disease progression, and both innate and adaptive immune mechanisms support and perpetuate hepatic inflammation in NASH. Previous studies have demonstrated that the pro-inflammatory leukotriene B4 (LTB4) is a potent chemoattractant that drives macrophage and neutrophil chemotaxis, and genetic loss or inhibition of its high affinity receptor, leukotriene B4 receptor 1 (BLT1), results in improved insulin sensitivity and decreased lipid accumulation in the liver. Accordingly, the LTB4-BLT1 axis is a potential therapeutic target for the treatment of liver steatosis and insulin resistance by modulating inflammation.The goal of this study is to validate the therapeutic efficacy of BLT1 inhibition in a NASH mouse model.
2023-11-25 | GSE248273 | GEO
Project description:The objective of this study was to compare the transcriptional repertoire of mature human neutrophils before and after GM-CSF treatment by using oligonucleotide microarrays. Leukotriene B4 (LTB4) is an important pro-inflammatory lipid mediator generated by neutrophils upon activation. Granulocyte/macrophage colony-stimulating factor (GM-CSF) stimulation is known to enhance agonist-mediated LTB4 production of neutrophils within minutes, a process called “priming”. Here, we demonstrate that GM-CSF also limits the production of LTB4 by neutrophils via a transcriptional mechanism at later time points. We identified hematopoietic specific Ras homologous (RhoH)/translocation three four (TTF), which was induced following GM-CSF stimulation in neutrophils, as a key regulator in this process. Neutrophils derived from RhoH/TTF-deficient (Rhoh-/-) mice demonstrated increased LTB4 production upon activation compared with normal mouse neutrophils. Moreover, neutrophils from cystic fibrosis patients expressed enhanced levels of RhoH/TTF and generated less LTB4 upon activation compared with normal human neutrophils. Taken together, these data suggest that RhoH/TTF represents an inducible feedback inhibitor in neutrophils that is involved in the limitation of innate immune responses.
2009-03-31 | GSE15139 | GEO
Project description:Cooperative and redundant signaling of leukotriene B4 and leukotriene D4 in human monocytes
| PRJNA132125 | ENA
Project description:Breast cancer cells facilitate distant metastasis through the induction of immunosuppressive regulatory B cells, designated tBregs. We report here that, to do this, breast cancer cells produce metabolites of the 5-lipoxygenase (5-LO) pathway such as leukotriene B4 (LTB4) to activate the proliferator-activated receptor alpha (PPARalpha) in B cells. Inactivation of LTB4 signaling or genetic deficiency of PPARalpha in B cells blocks the generation of tBregs and thereby abrogates lung metastasis in mice with established breast cancer. Thus, in addition to eliciting fatty acid oxidation and metabolic signals, PPARalpha initiates programs required for differentiation of tBregs. We propose that PPARalpha in B cells or/and tumor 5-LO pathways represents new targets for pharmacological control of tBreg-mediated cancer escape.
2013-03-13 | GSE43278 | GEO
Project description:Understanding pathogen recognition and mechanisms in Atlantic cod are of significant importance for both basic research on wild populations and health management in aquaculture. A microarray approach was utilized to search for effects of viral (poly I:C/ polyinosinic acid:polycytidylic acid), bacterial (LPS/lipopolysaccharide) and polyclonal activator (PHA-L/phytohaemoagglutinin) stress in Atlantic cod head kidney cells. LPS cell activation increased mRNA expression of chemokine/Interleukin 8 (CXCL8/IL-8); interleukin -1? (IL-1?); cyclooxygenase 2 (COX2); leukocyte derived chemotaxin 2 (LECT2); LOC100698154, encoding a protein with unknown function; carboxyl-esterase 2 (CES2) and environmental biomarker cytochrome P450 1A (CYP1A). Mitogen activated protein kinase p38 (p38MAPK) and cathepsin F (CTSF) were downregulated by LPS. The antiviral responses induced by double stranded RNA (Poly I:C) clearly increased transcription of Toll like receptor 3 (TLR3) and interferon stimulating gene 15 (ISG15). The PHA response seemed to be more non-specific. Special for the PHA induction were the increase in Major histocompatibility complex class I (MHCI). CC chemokine type 2 (CK2) mRNA expression was increased by PHA, LPS and poly I:C, while p38MAPK and LECT2 was downregulated by PHA. Oxidative stress related genes like catalase and glutaredoxin (GLRX2) and the anti-apoptotic gene Bcl-2 showed no transcriptional changes compared to control in any of the treatments. Especially Poly I:C, but also LPS, induced leukotriene B4 (LTB4) and leukotriene B5 (LTB5) synthesis, while small amounts of prostaglandine E2 (PGE2) seemed to be constitutively produced in untreated cells, a production that was slightly elevated when exposing cells for LPS. This study reveals distinct signatures of bacteria and virus transcriptional responses in cod head kidney cells. In addition, the novel finding that Cyp1a was upregulated during the antibacterial response indicates a connection between immunity and aryl hydrocarbon receptor (AhR) activation in Atlantic cod.
2012-03-21 | E-MTAB-1058 | biostudies-arrayexpress