Search results for: IL18
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2024/10/07
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Effect of inflammatory factors on myocardial infarction.
Cohort studies have increasingly shown associations between inflammatory markers and myocardial infarction (MI); however, the specific causal relationships between inflammatory markers and the development of MI remain unclear.Qingyi Zeng, Tao Xu, Zhenghua Luo, Haiyan Zhou, Zonggang Duan, Xinlin Xiong, Mengjun Huang, Wei Li
2943 related Products with: Effect of inflammatory factors on myocardial infarction.
9696 Tests/kit 2 ml 250ul5 x 200ul 6 ml Ready-to-use 10 μg5ug5ug100 units 25 ml
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#39372404 2024/09/20
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Epigenetic regulation in epithelial cells and innate lymphocyte responses to . Typhi infection: insights into IFN-γ production and intestinal immunity.
Infection by serovar Typhi (. Typhi), the cause of enteric fevers, is low in high-income countries but persistent in low- and middle-income countries, resulting in 65,400-187,700 deaths yearly. Drug resistance, including in the United States, exacerbates this issue. Evidence indicates that innate lymphocytes (INLs), such as natural killer (NK) cells, and unconventional T lymphocytes (., Mucosal-associated invariant T (MAIT) cells and T-cell receptor gamma delta (TCR-γδ) cells) can impact the intestinal epithelial barrier, the primary site of exposure to . Typhi. Moreover, INL production of IFN-γ is central in controlling . Typhi infection. However, the impact of epithelial cells (EC) on the secretion of IFN-γ by INLs and the relationship between these events and epigenetic changes remains unknown. Epigenetic modifications in host cells are fundamental for their differentiation and function, including IFN-γ production. Herein, using a human organoid-derived polarized intestinal epithelial cell monolayer, we investigated the role of H3K4me3 and H3K27me3 epigenetic marks in intestinal immunity, focusing on the function of EC, NK, MAIT, and TCR-γδ cells in response to . Typhi. This study builds on our previous findings that MAIT subsets exhibiting specific IFN-γ pattern signatures were associated with protection against typhoid fever and that . Typhi infection regulates changes in chromatin marks that depend on individual cell subsets. Here, we show that cultures exposed to . Typhi without EC exhibit a significant increase in NK and MAIT cells, and, to a lesser extent, TCR-γδ cells, expressing IFN-γ and H3K4me3 but not H3K27me3 marks, contrasting with cultures where EC is present. The influence of EC on INL H3K4me3 marks might be indirectly mediated through the modulation of IL-18 secretion via the Histone Deacetylase 6 gene during . Typhi infection.Rosângela Salerno-Goncalves, Haiyan Chen, Andrea C Bafford, Marcelo B Sztein
2678 related Products with: Epigenetic regulation in epithelial cells and innate lymphocyte responses to . Typhi infection: insights into IFN-γ production and intestinal immunity.
96 wells200 200 96 assays300 units1 g1 ml96 wells (1 kit)100ul100ug100ug Lyophilized100 extractions
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#39370783 2024/09/27
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Protein biomarkers in assessing kidney quality before transplantation‑current status and future perspectives (Review).
To meet the demand for kidney transplants (KTx), organs are frequently retrieved not only from standard criteria donors (SCD; a donor who is aged <50 years and suffered brain death from any number of causes, such as traumatic injuries or a stroke) but also from expanded criteria donors (any donor aged >60 years or donors aged >50 years with two of the following: A history of high blood pressure, a creatinine serum level ≥1.5 mg/dl or death resulting from a stroke). This comes at the cost of a higher risk of primary non‑function (the permanent hyperkalemia, hyperuremia and fluid overload that result in the need for continuous dialysis after KTx), delayed graft function (the need for dialysis session at least once during the first week after KTx), earlier graft loss and urinary complications (vesico‑ureteral reflux, obstruction of the vesico‑ureteral anastomosis, urine leakage). At present, there are no commercially available diagnostic tools for assessing kidney quality prior to KTx. Currently available predictive models based on clinical data, such as the Kidney Donor Profile Index, are insufficient. One promising option is the application of perfusion solutions for protein biomarkers of kidney quality and predictors of short‑ and long‑term outcomes. However, to date, protein markers that can be detected with ELISA, western blotting and cytotoxic assays have not been identified to be a beneficial predictors of kidney quality. These include lactate dehydrogenases, glutathione S‑transferases, fatty acid binding proteins, extracellular histones, IL‑18, neutrophil gelatinase‑associated lipocalin, MMPs and kidney injury molecule‑1. However, novel methods, including liquid chromatography‑mass spectrometry (LC‑MS) and microarrays, allow the analysis of all renal proteins suspended/dissolved in the acellular preservation solution used for kidney storage before KTx (including hypothermic machine perfusion as one of kidney storage methods) e.g. Belzer University of Wisconsin. Recent proteomic studies utilizing LC‑MS have identified complement pathway elements (C3, C1QB, C4BPA, C1S, C1R and C1RL), desmoplakin, blood coagulation pathway elements and immunoglobulin heavy variable 2‑26 to be novel predictors of kidney quality before transplantation. This was because they were found to correlate with estimated glomerular filtration rate at 3 and 12 months after kidney transplantation. However, further proteomic studies focusing on distinct markers obtained from hypothermic and normothermic machine perfusion are needed to confirm their predictive value and to improve kidney storage methods. Therefore, the present literature review from PubMed, Scopus, Embase and Web of Science was performed with the aims of summarizing the current knowledge on the most frequently studied single protein biomarkers. In addition, novel analytical methods and insights into organ injury during preservation were documented, where future directions in assessing organ quality before kidney transplantation were also discussed.Maksymilian Baryła, Michał Skrzycki, Roman Danielewicz, Maciej Kosieradzki, Marta Struga
1860 related Products with: Protein biomarkers in assessing kidney quality before transplantation‑current status and future perspectives (Review).
100ug Lyophilized100ug Lyophilized1 Set1 Set1 Set1 Set100ug Lyophilized100ul1 Set1 Set1 Set
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#39370514 2024/10/07
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Dietary ferulic acid supplementation enhances antioxidant capacity and alleviates hepatocyte pyroptosis in diquat challenged piglets.
Oxidative stress significantly impacts growth performance and liver function in piglets. Ferulic acid (FA) works as an antioxidant, however, the role and mechanism of FA in the regulation of diquat-induced oxidative stress in piglets are less known. This study was designed to investigate the effects of FA on growth performance and antioxidant capacity in piglets with diquat challenge.Junqiu Luo, Xiu Wu, Daiwen Chen, Bing Yu, Jun He
1258 related Products with: Dietary ferulic acid supplementation enhances antioxidant capacity and alleviates hepatocyte pyroptosis in diquat challenged piglets.
10 mg100ug Lyophilized 1 G96tests100ug100ug Lyophilized 1 G1 ml100ug Lyophilized100ug Lyophilized 1 G
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#39369806 2024/10/04
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Neuroprotection of celastrol against postoperative cognitive dysfunction through dampening cGAS-STING signaling.
Neuroinflammation is a central player in postoperative cognitive dysfunction (POCD), an intractable and highly confounding neurological complication with finite therapeutic options. Celastrol, a quinone methide triterpenoid, is a bioactive ingredient extracted from Tripterygium wilfordii with talented anti-inflammatory capacity. However, it is unclear whether celastrol can prevent anesthesia/surgery-evoked cognitive deficits in an inflammation-specific manner. The STING agonist 5,6-dimethylxanthenone-4-acetic acid (DMXAA) was used to determine whether celastrol possesses neuroprotection dependent on the STING pathway in vivo and in vitro. Isoflurane and laparotomy triggered cGAS-STING activation, caspase-3/GSDME-dependent pyroptosis, and enhanced Iba-1 immunoreactivity. Celastrol improved cognitive performance and decreased the levels of cGAS, 2'3'-cGAMP, STING, NFκB phosphorylation, Iba-1, TNFα, IL-6, and IFN-β. Downregulation of cleaved caspase-3 and N-GSDME was observed in the hippocampus of POCD mice and HT22 cells after celastrol administration, accompanied by limited secretion of pyroptosis-pertinent pro-inflammatory cytokines IL-1β and IL-18. DMXAA neutralized the favorable influences of celastrol on cognitive function, as confirmed by the activation of the STING/caspase-3/GSDME axis. These findings implicate celastrol as a therapeutic agent for POCD through anti-inflammation and anti-pyroptosis.Xueshan Bu, Hui Guo, Wenwei Gao, Lei Zhang, Jiabao Hou, Bixi Li, Zhongyuan Xia, Wei Wang
2848 related Products with: Neuroprotection of celastrol against postoperative cognitive dysfunction through dampening cGAS-STING signaling.
2 Pieces/Box1 mg7 inhibitors1.5 x 10^6 cells2 Pieces/Box 5 G2 Pieces/Box11 inhibitors5 mg2 Pieces/Box2 Pieces/Box
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#39368920 2024/10/04
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Interleukins in Urine and Blood as Markers of Infection and as Risk Factors for Systemic Conditions.
Interleukins are a diverse group of cytokines that play a crucial role in controlling immune responses and have potential as biomarkers. This mini review evaluates 12 recent papers linking urinary interleukins to both urinary infection and systemic diseases. While measurement of serum interleukins can indicate systemic inflammation, urinary interleukins provide more specific insights into renal or urinary tract inflammation. Urinary interleukins such as IL-8, IL-18, and IL-1β show promise for diagnosing urinary tract infections and other conditions. However, their diagnostic utility is complicated by their wide distribution in the body and patient-related factors. Advances in analytical techniques have enhanced the sensitivity and speed of interleukin measurement, improving their clinical utility. PATIENT SUMMARY: This review highlights research showing that measurement of molecules associated with the immune system in urine samples can help in diagnosing and monitoring disease affecting the urinary tract and kidneys. These urine tests can provide more specific information about infections than blood tests can.Richard Luxton, Janice Kiely, Marcus Drake
2358 related Products with: Interleukins in Urine and Blood as Markers of Infection and as Risk Factors for Systemic Conditions.
9696 samples96 Tests100 assays100 assays400Tests100 assays100 μg100 assays96 assays
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#39366291 2024/09/18
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Evaluating performance, intestinal lesions, and immunity related genes in heritage and modern broiler breeds during a necrotic enteritis challenge.
In this comparative study, the differential responses of heritage (ACRB; Athens Canadian Random Bred) and modern (Cobb) broilers to a necrotic enteritis (NE) challenge were evaluated. The design was a 2×2 factorial with breed (ACRB and Cobb) and challenge (non-challenged and NE-challenged) as main factors. On day (d) of hatch, 96 male chicks (48 ACRB and 48 Cobb) were allocated to 4 experimental groups with 8 replicate cages and 3 birds/cage. On d 14, birds in the NE-challenged groups were orally gavaged with 3,000 Eimeria maxima sporulated oocysts followed by 2 doses of ∼1×10 CFU of Clostridium perfringens on d 19 and 20. On d 21, 2 birds/cage were necropsied to score NE lesions, and spleen and cecal tonsils (CT) samples were collected from 1 bird/cage for assessing mRNA abundance. Challenged ACRB birds exhibited reduced growth performance and relative growth performance compared to challenged Cobb birds. There was no significant interaction between breed and challenge during the challenge period (d 14-21) for mortality. However, there was a challenge main effect (P ≤ 0.05) on mortality as manifested by greater NE-associated mortality compared to non-challenged birds. No significant breed × challenge interaction or breed main effect on lesion scores were observed in the duodenum, jejunum, and ileum. NE-challenged Cobb birds exhibited greater mRNA abundance of IL-18, TNFα, TLR1.2, TLR2.1, CCR5, CCR6, CCL20, and AvBD1 in CT compared to NE challenged ACRB birds. There was a significant breed × challenge interaction effect on mRNA abundance of IL-10, AvBD13, NK-Lysin, and LEAP2 in the spleen. Moreover, a main effect of breed was observed in IL-1β, IL-18, TNFα, TLR2.1, CCR5, CCL20, and NK-Lysin where ACRB birds had higher mRNA abundance than Cobb birds (P ≤ 0.05). The observed differences in performance, pathology, and mRNA abundance between ACRB and Cobb broilers during the NE challenge highlight the distinct immune response profiles of heritage and modern breeds, emphasizing the need for breed-specific nutritional, managerial, and genetic selection programs for modulating immune responses during enteric disease challenges.Laney E Froebel, Ali Calik, Nima K Emami, Candice E C Blue, Rami A Dalloul
1829 related Products with: Evaluating performance, intestinal lesions, and immunity related genes in heritage and modern broiler breeds during a necrotic enteritis challenge.
50 mg 100ul100ug25 mg2.5 mg100ul96T100ug Lyophilized10 mg100ul100ug
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#39367210 2024/10/04
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LncRNA MALAT1 to Enhance Pyroptosis in Viral Myocarditis Through UPF1-Mediated SIRT6 mRNA Decay and Wnt-β-Catenin Signal Pathway.
Viral myocarditis (VMC) is an inflammatory disease of the myocardium caused by cardioviral infection, especially coxsackievirus B3 (CVB3), and is a major contributor to acute heart failure and sudden cardiac death in children and adolescents. LncRNA MALAT1 knockdown reportedly inhibits the differentiation of Th17 cells to attenuate CVB3-induced VMC in mice. Moreover, long non-coding RNAs (lncRNAs) interact with RNA-binding proteins (RBPs) to regulate UPF1-mediated mRNA decay. However, it remains unclear whether MALAT1 can bind to UPF1 to mediate the mRNA decay of its target genes in VMC. Herein, we aimed to explore the effect of lncRNA MALAT1 on UPF1-mediated SIRT6 mRNA decay in VMC using in vivo and in vitro experiments. CVB3-infected BABL/C mice were used as VMC models, and MALAT1 interfering adenovirus was injected to achieve MALAT1 knockdown. The heart function of the VMC mice was assessed using echocardiography. Pathological changes in myocardial tissues were assessed after hematoxylin-eosin staining. Myocardial injury and inflammation were evaluated by measuring creatine kinase isoenzyme B, cardiac troponin T, interleukin (IL)-1β, and IL-18. TUNEL staining was performed to assess apoptosis in myocardial tissues. In vitro experiments were performed using H9c2 cells after transfection and CVB3 infection. The lactic dehydrogenase release, caspase-1 activity, and IL-1β and IL-18 levels in the cellular supernatant were detected. Western blotting was performed to determine the expression of pyroptosis-related proteins (GSDMD-N, NLRP3, ASC, and Cleaved-Caspase-1) and Wnt/β-catenin signal pathway-related proteins (Wnt1, β-catenin, and p-GSK-3β). RNA immunoprecipitation and RNA stability assays assessed the relationship between MALAT1, UPF1, and SIRT6. CVB3-infected mice and H9c2 cells exhibited elevated MALAT1 and reduced SIRT6 expression. MALAT1 knockdown or SIRT6 overexpression suppressed inflammation and pyroptosis and inhibited the activation of the Wnt/β-catenin signal pathway in myocardial tissues and cells. MALAT1 enhanced the enrichment of SIRT6 mRNA by UPF1 and disturbed the stability of SIRT6 mRNA to promote the development of VMC. MALAT1 can bind UPF1 to mediate SIRT6 mRNA decay and activate the Wnt/β-catenin signal pathway in VMC.Min Zeng, Zhi Chen, Yefeng Wang, Zhou Yang, Jinxing Xiang, Xiang Wang, Xun Wang
1997 related Products with: LncRNA MALAT1 to Enhance Pyroptosis in Viral Myocarditis Through UPF1-Mediated SIRT6 mRNA Decay and Wnt-β-Catenin Signal Pathway.
2 Pieces/Box2 Pieces/Box2 Pieces/Box2 Pieces/Box2 Pieces/Box2 Pieces/Box2 Pieces/Box2 Pieces/BoxInhibitors2 Pieces/Box2 Pieces/Box2 Pieces/Box
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#39367093 2024/10/04
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Non-pathogenic E. coli displaying decoy-resistant IL18 mutein boosts anti-tumor and CAR NK cell responses.
The tumor microenvironment can inhibit the efficacy of cancer therapies through mechanisms such as poor trafficking and exhaustion of immune cells. Here, to address this challenge, we exploited the safety, tumor tropism and ease of genetic manipulation of non-pathogenic Escherichia coli (E. coli) to deliver key immune-activating cytokines to tumors via surface display on the outer membrane of E. coli K-12 DH5α. Non-pathogenic E. coli expressing murine decoy-resistant IL18 mutein (DR18) induced robust CD8 T and natural killer (NK) cell-dependent immune responses and suppressed tumor progression in immune-competent colorectal carcinoma and melanoma mouse models. E. coli K-12 DH5α engineered to display human DR18 potently activated mesothelin-targeting chimeric antigen receptor (CAR) NK cells and enhance their trafficking into tumors, which extended survival in an NK cell treatment-resistant mesothelioma xenograft model by enhancing TNF signaling and upregulating NK activation markers. Our live bacteria-based immunotherapeutic system safely and effectively induces potent anti-tumor responses in treatment-resistant solid tumors, motivating further evaluation of this approach in the clinic.Shaobo Yang, Michal Sheffer, Isabel E Kaplan, Zongqi Wang, Mubin Tarannum, Khanhlinh Dinh, Yasmin Abdulhamid, Eden Bobilev, Roman Shapiro, Rebecca Porter, Robert Soiffer, Jerome Ritz, John Koreth, Yun Wei, Peiru Chen, Ke Zhang, Valeria Márquez-Pellegrin, Shanna Bonanno, Neel Joshi, Ming Guan, Mengdi Yang, Deng Li, Chiara Bellini, Fuguo Liu, Jianzhu Chen, Catherine J Wu, David Barbie, Jiahe Li, Rizwan Romee