Mouse Interleukin 18,IL-18 ELISA Kit
- Known as:
- Mouse Interleukin 18,Interleukin-18 Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- csb-e04609m
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Cusabio Elisa
- Gene target:
- Mouse Interleukin 18 IL-18 ELISA Kit
Related genes to: Mouse Interleukin 18,IL-18 ELISA Kit
- Gene:
- IL18 NIH gene
- Name:
- interleukin 18
- Previous symbol:
- -
- Synonyms:
- IGIF, IL1F4, IL-1g, IL-18
- Chromosome:
- 11q23.1
- Locus Type:
- gene with protein product
- Date approved:
- 1997-07-25
- Date modifiied:
- 2015-07-06
- Gene:
- IL18BP NIH gene
- Name:
- interleukin 18 binding protein
- Previous symbol:
- -
- Synonyms:
- IL18BPa
- Chromosome:
- 11q13.4
- Locus Type:
- gene with protein product
- Date approved:
- 1999-05-21
- Date modifiied:
- 2016-10-05
Related products to: Mouse Interleukin 18,IL-18 ELISA Kit
Related articles to: Mouse Interleukin 18,IL-18 ELISA Kit
- rapidly translocates across polarized human bronchial epithelial barriers, with viable bacteria recovered from the basolateral compartment within 1 h post-infection. Disruption of the pyruvate node through combined deletion of pyruvate oxidase ( ) and lactate oxidase ( ) markedly enhanced transmigration of across polarized Calu-3 monolayers without causing early cytotoxicity or loss of monolayer integrity. This hyper-invasive phenotype was conserved in the TIGR4 and EF3030 background and under air-liquid interface conditions. Importantly, single Δ mutants exhibited significantly greater translocation than Δ mutants or wild-type strains across bronchial (Calu-3), alveolar (A549), and pharyngeal (Detroit 562) epithelial models. Enhanced translocation correlated with increased bacterial adherence but was independent of capsule expression, extracellular H₂O₂ production, pneumolysin, or tight junction disruption, as evidenced by stable transepithelial electrical resistance (TEER), lack of caspase-3/7 activation, and minimal IL-18 release at early time points. High-resolution confocal microscopy revealed intracellular Δ pneumococci localized within N-acetylglucosamine/sialic acid (GN/SA)-containing compartments as early as 1 h post-infection. In murine macrophages, Δ mutants were phagocytosed at rates similar to wild-type bacteria but induced greater pneumolysin-dependent cytotoxicity at 24 h. These findings demonstrate that LctO functions as a metabolic checkpoint that restrains pneumococcal invasion of respiratory epithelia, revealing a previously unrecognized role for lactate oxidase in controlling the transition from colonization to invasive disease. - Source: PubMed
Publication date: 2026/07/16
Vidal Ana G JopTakeshita KenichiMurin LandonFlores-Vega Verónica RoxanaAlibayov BabekRosales-Reyes RobertoRosch Jason WBengten EvaVidal Jorge E - Physcion, a natural anthraquinone, possesses antifungal and anti-inflammatory activities. This study aimed to investigate its antifungal and anti-inflammatory effects in a murine model of Aspergillus fumigatus (AF) keratitis (AFK). - Source: PubMed
Publication date: 2026/07/28
Shi WenhaoXu HuirongXu QiangYang XuejiaoSun XiaoyanWan XiaomeiXue ShashaWang BingChe Chengye - Phthalates are a class of synthetic compounds, known as endocrine-disrupting chemicals, widely used as plasticizers in consumer products, including personal care items, medical devices, and food packaging. Two common phthalates, di(2-ethylhexyl) phthalate (DEHP) and diisononyl phthalate (DiNP), have been associated with adverse effects on female reproductive health. This study investigated the effects of acute DEHP and DiNP exposure on uterine inflammation and oxidative stress in adult female CD-1 mice. Mice were orally dosed for 10 days with vehicle control, DEHP (20μg/kg/day, 200μg/kg/day, or 200mg/kg/day), or DiNP (20μg/kg/day, 100μg/kg/day, or 200mg/kg/day). Uteri were collected during diestrus for histological and gene expression analyses. Quantitative PCR (qPCR) showed that DEHP (20 and 200μg/kg/day) and DiNP (200mg/kg/day) increased expression of inflammasome-related genes (Il18, Il1β, and Nlrp3). DiNP at 200mg/kg/day also increased Il10 expression. Oxidative stress genes revealed DEHP increased Prdx2 expression at all doses without affecting Sod1, Cat, or Gpx1. However, DiNP increased Prdx2 at 20μg/kg/day but reduced Sod1, Cat, and Gpx1 at higher doses. Histological analysis revealed that high-dose DiNP reduced outer myometrium thickness and luminal epithelial cell height, while DEHP only affected the cell height at the highest dose. Macrophage and other mononuclear phagocytic cell infiltration increased with DEHP (20 and 200μg/kg/day) and all doses of DiNP. while cell proliferation was only changed in DEHP (200μg/kg/day). Together, these findings demonstrate that acute exposure to DEHP and DiNP induces uterine inflammatory and oxidative stress responses, with distinct dose-dependent effects for each phthalate. - Source: PubMed
Publication date: 2026/07/28
Andrus Adriana RParra-Forero Lyda YSexton Coba NLiu Kalysta CRush Sarah MLaws Mary JFlaws Jodi ANowak Romana A - To study the effects of Polygonatum-Hedyotis diffusa on non-small cell lung cancer and the mechanism of action. - Source: PubMed
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Mao LeiJiang LingyingZhou YeXu ShouhangLou TingtingLu WeiyongZhu GaoyuanChen Jianwu - Bladder cancer remains a significant clinical challenge due to high recurrence and progression rates, necessitating novel therapeutic strategies. Oncolytic viruses, such as the herpes simplex virus type 2-based OHSV2, have demonstrated promising antitumor effects through direct oncolysis and immune activation. This study investigated the efficacy, safety, and molecular mechanisms of OHSV2 in the treatment of bladder cancer. In vitro and in vivo experiments demonstrated that OHSV2 potently inhibited bladder cancer cell proliferation, migration, and clonogenicity in a dose-dependent manner, while exhibiting a favorable safety profile. Critically, OHSV2 treatment triggered a pro-inflammatory tumor immune microenvironment, characterized by increased infiltration and activation of CD8 T cells. Mechanistically, OHSV2 induced pyroptosis in bladder cancer cells via the canonical Caspase-1/Gasdermin D (GSDMD) pathway, accompanied by increased interleukin-18 (IL-18), interleukin-1β (IL-1β), and lactate dehydrogenase (LDH) release. Further analysis identified NOD-like receptor family pyrin domain containing 3 (NLRP3) as the key upstream pattern recognition receptor for Caspase-1/GSDMD activation, and Toll-like receptor 4 (TLR4) as a critical mediator of NLRP3-dependent pyroptosis. Inhibition of TLR4 or NLRP3 partially reversed OHSV2-induced cytotoxicity, confirming their functional roles. Additionally, combining OHSV2 with the TLR4 agonist enhanced pyroptosis in a subcutaneous xenograft model, amplified antitumor immunity, and improved tumor control in vivo, suggesting potential synergism for clinical translation. These findings elucidate a novel TLR4/NLRP3/Caspase-1/GSDMD axis as the core mechanism behind the antitumor effect of OHSV2 and propose a rationale for its combination with immunomodulators to improve outcomes in bladder cancer. - Source: PubMed
Publication date: 2026/07/28
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