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Nucleotide-Binding Oligomerization Domain 1 (NOD1) Positively Regulates microglia-driven inflammatory response during Pseudorabies Virus Infection

ABSTRACT: Nucleotide-Binding Oligomerization Domain 1 (NOD1) Positively Regulates microglia-driven inflammatory response during Pseudorabies Virus Infection

PROVIDER: PRJNA1039482 | ENA |

REPOSITORIES: ENA

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Nucleotide-Binding Oligomerization Domain 1 (NOD1) Positively Regulates microglia-driven inflammatory response during Pseudorabies Virus Infection

Project description:The main cause of viral encephalitis is that the virus invades the central nervous system (CNS) and causes neuroinflammation, which poses a serious threat to the world’s public health. Microgliaare CNS-resident macrophages that playanimportantroleinneuroinflammation and thus often identified as target of choice for the prevention or treatment of viral encephalitis. Nucleotide-binding oligomerization domain 1 (NOD1) is a type of pattern recognition receptor and has been associated with many inflammatory diseases in humans. Here, we used pseudorabiesvirus (PRV) as a model to examine the regulation of microglia responses during viral encephalitis and discuss whether NOD1 suppressed neuroinflammation by regulating microglial activation. Cellular experiments indicated that microglia activation accompanying by cell migration, characteristic morphological changes, phagocytosis, inflammatory cytokine production and antigen presentation. We then investigated the effect of NOD1 on the PRV-induced microglia activation. Theresultsinvitro and in vivoshowedthat PRV infection upregulated the mRNA and protein expression of NOD1. Inhibition or overexpression of NOD1 can reduce or enhance the activation JNK and NF-κB signal pathway to regulate the microglia activation and inflammatory response induced by PRV.

2025-09-11 | GSE247533 | GEO

Gene expression in fetal aortic arteries of C57BL/6 mice with Nod1 stimulation

Project description:We previously demonstrated that an innate immune receptor, the nucleotide-binding oligomerization domain-1 (Nod1), was involved in the vascular disease in young and adult mice. However, little is known about the role of Nod1 signaling in fetuses. We administered FK565, one of the Nod1 ligands, to pregnant C57BL/6 mice and examined its effect in the fetuses. Nod1 stimulation increased levels of cytokines in the pregnant mice, placentae and fetuses. We found that FK565 which was administered to the pregnant mice transferred to the fetuses through the placentae, and exerted its effects on fetuses in vivo. Nod1 was abundantly expressed in the arteries, and the vascular tissues predominantly produced CCL2 and IL-6 in response to FK565 compared with other fetal tissues. FK565 induced up-regulation of genes associated with immune response, inflammation and apoptosis in fetal vascular tissues.

2016-01-31 | GSE65188 | GEO

Immune surveillance of cellular homeostasis by NOD1/2 via sensing cytosolic sphingosine-1-phosphate (S1P)

Project description:Chronic inflammation is associated with disruption of cellular homeostasis, yet the underlying mechanisms remain elusive1. Nucleotide-binding oligomerization domain-containing protein 1/2 (NOD1/2) are intracellular pathogen recognition receptors that activate innate immune responses via sensing bacterial peptidoglycans2-4. We demonstrate that NOD1/2 sense not only microbe-specific molecular patterns but also perturbation of cell homeostasis, and thereby cause inflammation. Host generation of sphingosine-1-phosphate (S1P) via the hydrolysis pathway is essential for NOD1/2 signaling upon such stress. Cytosolic delivery of S1P activates NOD1/2 dependent NF-κB activation and inflammation. Finally, we demonstrate that S1P directly binds to and activates NOD1/2. In sum, we describe a hitherto unknown role of NOD1/2 by revealing that they initiate innate immune responses by surveillance of cellular homeostasis through sensing of cytosolic S1P. Our findings provide a novel link between host cytosolic S1P and NOD1/2 mediated immune activation upon perturbation of cellular homeostasis and thus form the basis for future intervention strategies targeting the S1P-NOD1/2 axis.

2020-01-01 | GSE124828 | GEO

Zebrafish embryos microinjected with ptGFP1 (control group) or ptGFP1-NOD1 (NOD1 group)

Project description:Transcriptional profiling of zebrafish embryos comparing control group microinjected with empty plasmid with NOD1 group microinjected with ptGFP1-NOD1 plasmid.

2018-06-22 | GSE116109 | GEO

NLR Nod1 signaling promotes survival of BCR-engaged mature B cells through upregulated Nod1 as a positive outcome

Project description:BCR ligand-engaged B cells upregulate Nod1 during development. Most mature B cells have up-regulated Nod1 and are sensitive to Nod1 signaling, which increases survival upon exposure to microbial products, as a positive outcome of BCR-engaged mature B cells.

2017-09-03 | GSE101318 | GEO

Mouse atrial tissue quantitative proteomics

Project description:Project description: Proteomics study of the role of nucleotide oligomerization domain type 1 (NOD1) in a mouse model of heart failure. A high-throughput quantitative proteomic analysis was performed in atrial myocardium obtained from Wt- and Nod1-/--Tac mice and their respective Sham groups.

2025-07-17 | PXD053998 | JPOST Repository

Microbial-ligand independent regulation of lymphpoiesis by NOD1

Project description:Aberrant differentiation of progenitor cells in the hematopoietic system is known to severely impact host immune responsiveness. Here we demonstrate that NOD1, a cytosolic innate sensor of bacterial peptidoglycan, also functions in murine hematopoietic cells as a major regulator of both the generation and differentiation of lymphoid progenitors as well as peripheral T lymphocyte homeostasis. We further show that NOD1 mediates these functions by facilitating STAT5 signaling downstream of hematopoietic cytokines. In steady-state, loss of NOD1 resulted in a modest but significant decrease in numbers of mature T, B and NK cells. During systemic protozoan infection, this defect was markedly enhanced leading to host mortality. Lack of functional NOD1 also impaired T-cell-dependent anti-tumor immunity while preventing colitis. These findings reveal that in addition to its classical role as a bacterial ligand receptor, NOD1 plays an important function in regulating adaptive immunity through interaction with a major host cytokine signaling pathway.

2023-10-25 | GSE236485 | GEO

Zebrafish embryos microinjected with ptGFP1 (control group) or ptGFP1-NOD1 (NOD1 group)

Project description:Zebrafish embryos microinjected with ptGFP1 (control group) or ptGFP1-NOD1 (NOD1 group)

| PRJNA477292 | ENA

Characterization of Rabbit Nucleotide-Binding Oligomerization Domain 1 (NOD1) and the Role of NOD1 Signaling Pathway during Bacterial Infection.

Project description:Nucleotide-binding oligomerization domain 1 (NOD1) is the most prominent of all NOD-like receptors, which in the mammalian innate immune system, serve as intracellular receptors for pathogens and endogenous molecules during tissue injury. From rabbit kidney cells, we cloned rabbit NOD1 (rNOD1) and identified an N-terminal caspase activation and recruitment domain, a central NACHT domain, and C-terminal leucine-rich repeat domains. rNOD1 was expressed in all tested tissues; infection with Escherichia coli induced significantly higher expression in the spleen, liver, and kidney compared to other tissues. The overexpression of rNOD1 induced the expression of proinflammatory cytokines Il1b, Il6, Il8, Ifn-γ, and Tnf and defensins, including Defb124, Defb125, Defb128, Defb135, and Np5 via activation of the nuclear factor (NF)-κB pathway. Overexpression of rNOD1 inhibited the growth of E. coli, whereas knockdown of rNOD1 or inhibition of the NF-κB pathway promoted the growth of E. coli. rNOD1 colocalized with LC3, upregulated autophagy pathway protein LC3-II, and increased autolysosome formation in RK-13 cells infected with E. coli. In summary, our results explain the primary signaling pathway and antibacterial ability of rNOD1, as well as the induction of autophagy that it mediates. Such findings suggest that NOD1 could contribute to therapeutic strategies such as targets of new vaccine adjuvants or drugs.

| S-EPMC5641294 | biostudies-literature

Effects of Pseudorabies Virus Infection on the Tracheobronchial Lymph Node Transcriptome

Project description:RNA isolated from draining tracheobronchial lymph nodes (TBLN) from 5-week old pigs, either clinically infected with a feral isolate of Pseudorabies virus or uninfected were interrogated using Illumina Digital Gene Expression Tag Profiling. Over 100 million tag sequences were observed, representing 4,064,189 unique 21-base sequences collected from TBLN at time points 1, 3, 6 and 14 days post-infection (dpi) RNA isolated from draining tracheobronchial lymph nodes (TBLN) from 5-week old pigs (% per group pooled), either clinically infected with feral isolate FS268 of Pseudorabies virus or uninfected at 1, 3, 6, and 14 days post inoculation. Over 100 million tag sequences were observed, representing 4,064,189 unique 21-base sequences.

2015-10-30 | E-GEOD-74473 | biostudies-arrayexpress

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