Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Elevation of IL-8 secretion induced by PEDV infection via NF-κB signaling pathway.

ABSTRACT: Porcine epidemic diarrhea virus (PEDV) is associated with severe enteritis, which contributes to high mortality in piglets. The aim of this study was to describe molecular mechanisms associated with proinflammatory cytokine(s) production during PEDV infection. We showed that infection of porcine intestine epithelial cell clone J2 (IPEC-J2) with PEDV induces a gradual increase in interleukin 8 (IL-8) production at different time points, as well as infection of Vero E6 with PEDV. The secretion of IL-8 in these two cell lines infected with PEDV is related to the activation of NF-κB. Furthermore, the cells expressing PEDV M or E protein can induce the upregulation of IL-8. These findings suggest that the IL-8 production can be the initiator of inflammatory response by the host cells upon PEDV infection.

SUBMITTER: Wu Y

PROVIDER: S-EPMC11298435 | biostudies-literature | 2024

REPOSITORIES: biostudies-literature

ACCESS DATA

Json Xml

Publications

Elevation of IL-8 secretion induced by PEDV infection via NF-κB signaling pathway.

Wu Yang Y Wang Yongrui Y Wang Xuepeng X Li Mingwei M Yan Haoxin H Shi Hongyan H Shi Da D Chen Jianfei J Guo Longjun L Feng Li L

Frontiers in cellular and infection microbiology 20240722

Porcine epidemic diarrhea virus (PEDV) is associated with severe enteritis, which contributes to high mortality in piglets. The aim of this study was to describe molecular mechanisms associated with proinflammatory cytokine(s) production during PEDV infection. We showed that infection of porcine intestine epithelial cell clone J2 (IPEC-J2) with PEDV induces a gradual increase in interleukin 8 (IL-8) production at different time points, as well as infection of Vero E6 with PEDV. The secretion of ...[more]

PMID: 39104852

Similar Datasets

Paeoniflorin inhibits IL-1β-induced MMP secretion via the NF-κB pathway in chondrocytes.

Project description:Paeoniflorin serves important cellular roles, exerting anti-cancer, anti-inflammatory and anti-pulmonary fibrosis effects and possesses immune-modulatory properties. However, the exact role of paeoniflorin in the pathogenesis of osteoarthritis (OA) remains unclear. The aim of the present study was to investigate the effects of paeoniflorin on articular surfaces in vitro. Rat chondrocytes were cultured in vitro and an MTT assay was performed to assess chondrocyte survival. Following treatment with interleukin (IL)-1β and paeoniflorin, the production of matrix metalloproteinases (MMPs) and tissue inhibitor of metalloproteinases-1 (TIMP-1) was examined using reverse transcription-quantitative polymerase chain reaction and western blotting. The interleukin (IL)-1β-induced nuclear factor (NF)-κB pathway activation was also investigated. The results demonstrated that paeoniflorin was able to downregulate the expression of MMP and increase the expression of TIMP-1ntmRNA and protein in IL-1β-induced rat chondrocytes. Furthermore, treating chondrocytes with paeoniflorin blocked the activation of NF-κB. These results suggest that paeoniflorin may serve am anti-catabolic role in the progression of OA and may be an effective preventative treatment for OA.

| S-EPMC6090372 | biostudies-literature

Herpesvirus latent infection promotes stroke via activating the OTUD1/NF-κB signaling pathway.

Project description:ObjectiveOur study aimed to reveal the molecular mechanisms underlying the regulation of cerebral infarction by herpes virus latency infection via the OTUD1/NF-κB signaling pathway using evidence-based medicine Meta-analysis and bioinformatics analysis.MethodsWe conducted a Meta-analysis by searching Pubmed, Embase, and Web of Science databases to evaluate the correlation between herpes virus infection and increased risk of cerebral infarction. We obtained wild-type or mutant herpes virus latent infection-related brain tissue datasets from the GEO database and performed differential analysis to identify differentially expressed genes (DEGs) in the brain tissue after herpes virus latent infection. We further conducted WGCNA co-expression analysis on the cerebral infarction-related datasets from the GEO database to obtain key module genes and intersect them with the DEGs. We used ROC curve analysis to identify the key gene OTUD1 for predicting the occurrence of cerebral infarction and combined correlation and pathway enrichment analyses to identify the downstream pathways regulated by OTUD1.ResultsOur meta-analysis revealed that herpes virus infection is associated with an increased risk of cerebral infarction. By integrating the differential analysis and WGCNA co-expression analysis of GEO chip data, we identified three key genes mediating cerebral infarction after herpes virus latent infection. ROC curve analysis identified the key gene OTUD1, and the correlation and pathway enrichment analyses showed that OTUD1 regulates the NF-κB signaling pathway to mediate cerebral infarction.ConclusionHerpes virus latent infection promotes cerebral infarction by activating the OTUD1/NF-κB signaling pathway.

| S-EPMC10522389 | biostudies-literature

NCOA2-induced secretion of leptin leads to fetal growth restriction via the NF-κB signaling pathway.

Project description:BackgroundFetal growth restriction (FGR) is one of the most common fetal complications during pregnancy in the obstetrics department, with poor therapeutic efficacy. The local inflammatory response of the placenta has gradually become known as the main mechanism for the occurrence and development of FGR. The aim of this study was to improve the knowledge of placental inflammatory response mechanisms in regulating gene expression.MethodsThe differentially expressed genes (DEGs) in FGR patients were analyzed through bioinformatics analysis. The expression of gene level was detected by immunohistochemistry (IHC) staining, quantitative polymerase chain reaction (qPCR), or enzyme-linked immunosorbent assay (ELISA). The proliferation, migration, and apoptosis of HTR-8/SVneo trophoblast cells stimulated with lipopolysaccharide (LPS) was performed by Cell Counting Kit-8 (CCK-8) assay, clone formation assay, Transwell assay, and flow cytometry. The mechanisms of gene expression in regulating placental inflammatory response were elucidated by western blotting.ResultsNuclear receptor coactivator 2 (NCOA2) was identified as a very critical gene in the progression of FGR by bioinformatics analysis and the expression of NCOA2 was shown to be down-regulated in FGR patients. Overexpression of NCOA2 promoted the proliferation, migration, and inhibited apoptosis and pro-inflammatory cytokines secretion in HTR-8/SVneo trophoblast cells stimulated with LPS via the nuclear factor (NF)-κB pathway. In addition, leptin was increased in both tissue and peripheral blood samples of FGR patients, and overexpression of NCOA2 inhibited the secretion of leptin in HTR-8/SVneo trophoblast cells stimulated with LPS.ConclusionsAll these findings suggest that NCOA2-induced secretion of leptin leads to FGR progression via the NF-κB pathway and provides a clinical therapeutic target in FGR and a potent marker for the identification of FGR.

| S-EPMC10009567 | biostudies-literature

Lipocalin 2 potentially contributes to tumorigenesis from colitis via IL-6/STAT3/NF-κB signaling pathway.

Project description:Lipocalin (LCN) 2 (LCN2), a member of the lipocalin superfamily, plays an important role in oncogenesis and progression in various types of cancer. However, the role of LCN2 in inflammation-associated cancer remains unknown. Here, we explored the functional role and mechanisms of LCN2 in tumorigenesis using murine colitis-associated cancer (CAC) models and human colorectal cancer (CRC) cells. Using murine CAC models, we found that LCN2 was preferentially expressed in colonic tissues from CAC models compared with tissues from normal mice. In vitro results demonstrated that the levels of LCN2 mRNA and protein were markedly up-regulated by interleukin (IL) 6 (IL-6) in human CRC cells. Interestingly, we found LCN2 up-regulation by IL-6 is diminished by nuclear factor-κB (NF-κB) and signal transducer and activator of transcription 3 (STAT3) inhibition using specific inhibitors and small interfering RNA (siRNA). Reporter assay results determined that IL-6 induces LCN2 gene promoter activity under control of NF-κB/STAT3 activation. IL-6-induced LCN2 regulated cell survival and susceptibility of developmental factors to the NF-κB/STAT3 pathway. Taken together, our results highlight the unknown role of LCN2 in CAC progression and suggest that increased LCN2 may serve as an indicator of CRC development in the setting of chronic inflammation.

| S-EPMC9109459 | biostudies-literature

Non-canonical NF-κB signaling pathway.

Project description:The non-canonical NF-κB pathway is an important arm of NF-κB signaling that predominantly targets activation of the p52/RelB NF-κB complex. This pathway depends on the inducible processing of p100, a molecule functioning as both the precursor of p52 and a RelB-specific inhibitor. A central signaling component of the non-canonical pathway is NF-κB-inducing kinase (NIK), which integrates signals from a subset of TNF receptor family members and activates a downstream kinase, IκB kinase-α (IKKα), for triggering p100 phosphorylation and processing. A unique mechanism of NIK regulation is through its fate control: the basal level of NIK is kept low by a TRAF-cIAP destruction complex and signal-induced non-canonical NF-κB signaling involves NIK stabilization. Tight control of the fate of NIK is important, since deregulated NIK accumulation is associated with lymphoid malignancies.

| S-EPMC3193406 | biostudies-other

<i>A. caviae</i> infection triggers IL-1β secretion through activating NLRP3 inflammasome mediated by NF-κB signaling pathway partly in a TLR2 dependent manner.

Project description:Aeromonas caviae, an important food-borne pathogen, induces serious invasive infections and inflammation. The pro-inflammatory IL-1β functions against pathogenic infections and is elevated in various Aeromonas infection cases. However, the molecular mechanism of A. caviae-mediated IL-1β secretion remains unknown. In this study, mouse macrophages (PMs) were used to establish A. caviae infection model and multiple strategies were utilized to explore the mechanism of IL-1β secretion. IL-1β was elevated in A. caviae infected murine serum, PMs lysates or supernatants. This process triggered NLRP3 levels upregulation, ASC oligomerization, as well as dot gathering of NLRP3 and speck-like signals of ASC in the cytoplasm. MCC950 blocked A. caviae mediated IL-1β release. Meanwhile, NLRP3 inflammasome mediated the release of IL-1β in dose- and time-dependent manners, and the release of IL-1β was dependent on active caspase-1, as well as NLRP3 inflammasome was activated by potassium efflux and cathepsin B release ways. A. caviae also enhanced TLR2 levels, and deletion of TLR2 obviously decreased IL-1β secretion. What's more, A. caviae resulted in NF-κB p65 nuclear translocation partly in a TLR2-dependent manner. Blocking NF-κB using BAY 11-7082 almost completely inhibited NLRP3 inflammasome first signal pro-IL-1β expression. Blocking TLR2, NF-κB, NLRP3 inflammasome significantly downregulated IL-1β release and TNF-α and IL-6 levels. These data illustrate that A. caviae caused IL-1β secretion in PMs is controlled by NLRP3 inflammasome, of which is mediated by NF-κB pathway and is partially dependent on TLR2, providing basis for drugs against A. caviae.

| S-EPMC9450903 | biostudies-literature

Pioglitazone ameliorates neuronal damage after traumatic brain injury via the PPARγ/NF-κB/IL-6 signaling pathway.

Project description:Traumatic brain injury (TBI) is the major cause of high mortality and disability rates worldwide. Pioglitazone is an activator of peroxisome proliferator-activated receptor-gamma (PPARγ) that can reduce inflammation following TBI. Clinically, neuroinflammation after TBI lacks effective treatment. Although there are many studies on PPARγ in TBI animals, only few could be converted into clinical, since TBI mechanisms in humans and animals are not completely consistent. The present study, provided a potential theoretical basis and therapeutic target for neuroinflammation treatment after TBI. First, we detected interleukin-6 (IL-6), nitric oxide (NO) and Caspase-3 in TBI clinical specimens, confirming a presence of a high expression of inflammatory factors. Western blot (WB), quantitative real-time PCR (qRT-PCR) and immunohistochemistry (IHC) were used to detect PPARγ, IL-6, and p-NF-κB to identify the mechanisms of neuroinflammation. Then, in the rat TBI model, neurobehavioral and cerebral edema levels were investigated after intervention with pioglitazone (PPARγ activator) or T0070907 (PPARγ inhibitor), and PPARγ, IL-6 and p-NF-κB were detected again by qRT-PCR, WB and immunofluorescence (IF). The obtained results revealed that: 1) increased expression of IL-6, NO and Caspase-3 in serum and cerebrospinal fluid in patients after TBI, and decreased PPARγ in brain tissue; 2) pioglitazone could improve neurobehavioral and reduce brain edema in rats after TBI; 3) the protective effect of pioglitazone was achieved by activating PPARγ and reducing NF-κB and IL-6. The neuroprotective effect of pioglitazone on TBI was mediated through the PPARγ/NF-κB/IL-6 pathway.

| S-EPMC7083749 | biostudies-literature

TRIM14 promotes endothelial activation via activating NF-κB signaling pathway.

Project description:Endothelial activation by proinflammatory cytokines is closely associated to the pathogenesis of atherosclerosis and other vascular diseases; however, the molecular mechanisms controlling endothelial activation are not fully understood. Here we identify TRIM14 as a new positive regulator of endothelial activation via activating NF-κB signal pathway. TRIM14 is highly expressed in human vascular endothelial cells (ECs) and markedly induced by inflammatory stimuli such as TNF-α, IL-1β, and LPS. Overexpression of TRIM14 significantly increased the expression of adhesion molecules such as VCAM-1, ICAM-1, E-selectin, and cytokines such as CCL2, IL-8, CXCL-1, and TNF-α in activated ECs and by which it facilitated monocyte adhesion to ECs. Conversely, knockdown of TRIM14 has opposite effect on endothelial activation. Upon TNF-α stimulation, TRIM14 is recruited to IKK complex via directly binding to NEMO and promotes the phosphorylation of IκBα and p65, which is dependent on its K63-linked ubiquitination. Meanwhile, p65 can directly bind to the promoter regions of human TRIM14 gene and control its mRNA transcription. Finally, TRIM14 protein level is significantly upregulated in mouse and human atheroma compared to normal arteries. Taken together, these results indicate that TRIM14-NF-κB forms a positive feedback loop to enhance EC activation and TRIM14 may be a potential therapeutic target for vascular inflammatory diseases such as atherosclerosis.

| S-EPMC7181718 | biostudies-literature

Glycyrrhizin Inhibits PEDV Infection and Proinflammatory Cytokine Secretion via the HMGB1/TLR4-MAPK p38 Pathway.

Project description:Our previous study showed that glycyrrhizin (GLY) inhibited porcine epidemic diarrhea virus (PEDV) infection, but the mechanisms of GLY anti-PEDV action remain unclear. In this study, we focused on the anti-PEDV and anti-proinflammatory cytokine secretion mechanisms of GLY. We found that PEDV infection had no effect on toll-like receptor 4 (TLR4) protein and mRNA levels, but that TLR4 regulated PEDV infection and the mRNA levels of proinflammatory cytokines. In addition, we demonstrated that TLR4 regulated p38 phosphorylation but not extracellular regulated protein kinases1/2 (Erk1/2) and c-Jun N-terminal kinases (JNK) phosphorylation, and that GLY inhibited p38 phosphorylation but not Erk1/2 and JNK phosphorylation. Therefore, we further explored the relationship between high mobility group box-1 (HMGB1) and p38. We demonstrated that inhibition of HMGB1 using an antibody, mutation, or knockdown decreased p38 phosphorylation. Thus, HMGB1 participated in activation of p38 through TLR4. Collectively, our data indicated that GLY inhibited PEDV infection and decreased proinflammatory cytokine secretion via the HMGB1/TLR4-mitogen-activated protein kinase (MAPK) p38 pathway.

| S-EPMC7215578 | biostudies-literature

Eugenol modulates the NOD1- NF-κB signaling pathway via targeting NF-κB protein in triple breast cancer cells

Project description:Background: The most aggressive subtype of breast cancer, triple-negative breast cancer (TNBC), has a worse prognosis and a higher probability of relapse since there is a narrow range of treatment options. Identifying and testing potential therapeutic targets for the treatment of TNBC is of high priority. Methods: Using a transcriptional signature of triple-negative breast cancer collected from Gene Expression Omnibus (GEO), CMap was utilized to reposition compounds for the treatment of TNBC. CCK8 and colony formation experiments were performed to detect the effect of the candidate drug on the proliferation of TNBC cells, while flow cytometry was used to detect cell apoptosis. Meanwhile, transwell assay was implemented to detect cell metastasis change caused by the candidate drug. Moreover, the proteomic approach was presently ongoing to evaluate the underlying mechanism of the candidate drug in TNBC. Furthermore, drug affinity responsive target stability (DARTS) coupled with LC-MS/MS was carried out to explore the potential drug target candidate in TNBC cells. Results: We found that the most widely used medication, eugenol, reduced the growth and metastasis of TNBC cells. According to the underlying mechanism revealed by proteomics, eugenol could inhibit TNBC cell proliferation via the NOD1-NF-κB signaling pathway. DARTS experiment further revealed that eugenol may bind to NF-κB in TNBC cells. Concludes: Our findings pointed out that eugenol was a potential candidate drug for the treatment of TNBC.

2023-05-10 | PXD039305 | Pride

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data