Nod2
- Known as:
- Nod2
- Catalog number:
- 000055A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- Nod2
Related genes to: Nod2
- Gene:
- NOD2 NIH gene
- Name:
- nucleotide binding oligomerization domain containing 2
- Previous symbol:
- IBD1, CARD15
- Synonyms:
- BLAU, CD, PSORAS1, CLR16.3, NLRC2
- Chromosome:
- 16q12.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-07-10
- Date modifiied:
- 2019-04-23
Related products to: Nod2
Related articles to: Nod2
- Sepsis is a life-threatening condition characterized by severe organ dysfunction resulting from an uncontrolled host response to infection. Sepsis treatment poses a challenge due to its complexity and the need for effective therapeutic approaches. The objective of this study was to evaluate the immunomodulatory and antimicrobial effects of exopolysaccharides (EPS) from Auricularia auricula in a murine model of lethal sepsis. Our findings demonstrated that treatment with EPS significantly enhances the proliferation of circulating lymphocytes and granulocytes, which is associated with improved host defense mechanisms. Additionally, EPS administration effectively mitigates sepsis-induced pulmonary damage, as evidenced by preserved lung function. Furthermore, EPS treatment significantly reduces microbial translocation to the bloodstream, maintaining a lower colony-forming unit (CFU) count and thereby restricting systemic infection. The polysaccharides also prevent the development of thrombocytopenia in septic animals, thereby preserving platelet homeostasis. The compound modulates serum cytokine profiles, contributing to a more regulated inflammatory response. The interactome analysis reveals that the Dectin-1 → Syk pathway activates NF-κB/AP-1 and involves p38 MAPK, thereby explaining the observed cytokine modulation. The presence of Nod2/Ripk2 suggests that the EPS primes leukocytes to effectively combat both fungi and bacteria, leading to a reduced bacterial load and increased survival. Collectively, these data indicate that EPS, a prebiotic agent, represents a novel therapeutic strategy with potential for modulating immune responses, controlling microbial proliferation, and improving survival outcomes in a model of severe sepsis. - Source: PubMed
Viana Jesse Pereira MachadoCoelho Luisa CoutinhoMendes Priscila MVale André Alvares MarquesCasarin Jeferson NoslenSousa Joicy Cortez de SáPereira Paulo Vitor SoeiroLeal Maria Carolina B Di MedeirosBocca Anamelia LMaciel Márcia C G - Inflammation driven by the innate immune response plays a crucial role in osteoarthritis (OA) pathogenesis, yet the underlying mechanisms remain incompletely understood. Moreover, current antiinflammatory therapies primarily offer symptomatic relief without altering disease progression. Nucleotide-binding oligomerization domain 2 (NOD2) is an intracellular pattern recognition receptor that detects a broad range of microbial and damage-associated stimuli and has been implicated in several inflammatory conditions. In this study, we investigated the role of NOD2 in OA-associated inflammation and cartilage degradation. Elevated NOD2 expression was observed in both human and mouse osteoarthritic cartilage. Conditional KO of Nod2 in chondrocytes suppressed inflammation-induced catabolic responses in vitro and protected against cartilage degradation in mouse OA models. Mechanistically, we identified tumor necrosis factor receptor-associated factor 6 (TRAF6) as a key downstream mediator through which NOD2 promotes chondrocyte catabolism. Furthermore, we showed that pharmacological inhibition of NOD2 using 2 independent small-molecule inhibitors significantly attenuated OA progression in vivo. Collectively, these findings establish NOD2 as a critical regulator of OA-associated inflammation and cartilage degradation, and they highlight its potential as a therapeutic target for disease-modifying OA treatment. - Source: PubMed
Publication date: 2026/08/24
Wang YutingLi SongDong YonghuiZhang JiamingLiu JianWang ZhenggangLiang ShuangMartinez Nathan RPu HongxuCheng PengChen AnminYang QingChan Charles KfJiang WenXiao JunGuo FengjingZhao Liming - Lactiplantibacillus plantarum is a metabolically versatile lactic acid bacterium found in fermented foods and the human gastrointestinal tract. Its relatively large genome (3.0-3.6 Mb) features an open pan-genome with 1,436-2,100 core genes and over 13,000 cloud genes, enabling remarkable adaptation to diverse environments. This species encodes a diverse repertoire of CAZymes that degrade plant polysaccharides and host glycans, yielding short-chain fatty acids that modulate epithelial barrier integrity, host metabolism, and immune signaling. Pattern-recognition receptors (PRRs, including TLR2, TLR9, and NOD2) detect L. plantarum at the host interface, primarily through cell-surface molecules such as lipoteichoic acids, peptidoglycan, and exopolysaccharides. These interactions can influence NF-κB signaling, leading to either inflammatory or regulatory responses, depending on the specific strain. Certain strains also possess the glutamate decarboxylase system (GadB/GadC), which transforms dietary glutamate into gamma-aminobutyric acid (GABA), linking L. plantarum to the biology of the gut-brain axis. Despite substantial mechanistic evidence, clinical outcomes are inconsistent due to the significant variability among strains, marked differences in host microbiomes, and the absence of predictive multiomic markers for colonization and efficacy. This review consolidates current insights on genome organization, metabolic characteristics, and mechanisms of host interaction, with a specific focus on the challenges that continue to hinder the advancement of L. plantarum as a precision biotherapeutic. - Source: PubMed
Publication date: 2026/08/21
Chen YongRizwan MuhammadNawaz AsifWaheed Muhammad IhteshamWaqas MuhammadUllah Mati - Newcastle disease virus (NDV), a significant avian paramyxovirus, depends on the acquisition of host-derived membranes for viral envelope assembly during budding. However, the relationship between NDV budding efficiency and host metabolic reprogramming remains incompletely understood. Our previous research demonstrated that the highly virulent strain Herts/33 and the non-virulent strain LaSota differ significantly in budding efficiency, which is attributed to the difference in ubiquitination levels at the K247 site of the M protein. In this study, using recombinant viruses generated in our previous study, we investigated the effects of the K247 ubiquitination site on host cell metabolism. Through RNA sequencing and LC-MS/MS, systematically profiled the transcriptional and metabolic alterations induced by these viruses in HeLa cells. We also compared organ pathology in three-week-old SPF chicks infected with Herts/33 versus LaSota. The results showed that NDV infection broadly reprograms host sphingolipid metabolism. Compared with rLaSota-WT, rLaSota-R247K exhibited higher budding efficiency, linked to accelerated ceramide depletion and a stronger innate immune response. Specifically, rLaSota-R247K infection upregulated interferon- and interleukin-related components such as ISG15, CXCL8, TNF-α, CXCL10, NOD2, CD274, OAS, and IFNB1. Furthermore, we confirmed that blocking the ceramide synthesis pathway significantly suppresses NDV-M protein-mediated budding of VLPs and virions. Pathologically, Herts/33 induced more severe tissue damage than LaSota. Together, these findings indicate that the K247 residue of the NDV M protein enhances viral budding and promotes rapid utilization of host sphingolipids. This work provides mechanistic insight into NDV budding and highlights virus-host metabolic interactions that may inform future antiviral strategies. - Source: PubMed
Publication date: 2026/08/03
Dai JunLiu FanxinFeng YiyiYou QinqinWang JiaojiaoDing ChanQiu XushengXiao Shiji - This narrative review synthesizes current evidence on the immunopathogenesis of autoimmune uveitis(AU), with particular emphasis on genetic susceptibility, immunometabolic dysregulation, tissue-resident immunity, and the proposed gut-spleen-eye immunometabolic axis. - Source: PubMed
Publication date: 2026/08/18
Lin LipingZhang JingqiXie Xuejun