Category: Publication Spotlight

The Eagle Bioscience’s Mouse PD-L1 ELISA Kit was highlighted in a recent publication that explored gene guided OX40L expression on tumor cells to initiate tumor “self-killing”. Check out the full text and abstract below.

Abstract

The low objective response rates and severe side effects largely limit the clinical outcomes of immune checkpoint blockade (ICB) therapy. Here, a tumor “self-killing” therapy based on gene-guided OX40L anchoring to tumor cell membrane was reported to boost ICB therapy. We developed a highly efficient delivery system HA/PEI-KT (HKT) to co-deliver the OX40L plasmids and unmethylated CG-enriched oligodeoxynucleotide (CpG). On the one hand, CpG induced the expression of OX40 on T cells within tumors. On the other hand, OX40L plasmids achieved the OX40L anchoring on the tumor cell membrane to next promote T cells responses via OX40/OX40L axis. Such synergistic tumor “self-killing” strategy finally turned “cold” tumors to “hot”, to sensitize tumors to programmed cell death protein 1/programmed cell death ligand 1 (PD-1/PD-L1) blockade therapy, and promoted an immune-mediated tumor regression in both B16F10 and 4T1 tumor models, with prevention of tumor recurrence and metastasis. To avoid the side effects, the gene-guided OX40L anchoring and PD-L1 silencing was proposed to replace the existing antibody therapy, which showed negligible toxicity in vivo. Our work provided a new possibility for tumor “self-killing” immunotherapy to treated various solid tumors.

Lin, Lin, et al. “Gene-Guided OX40L Anchoring to Tumor Cells for Synergetic Tumor ‘Self-Killing’ Immunotherapy.” Bioactive Materials, 2022, https://doi.org/10.1016/j.bioactmat.2022.07.008.

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The Eagle Bioscience’s 25-OH Vitamin D ELISA Assay was highlighted in a recent publication that explored the relationship between vitamin D and leptin hormones in type 2 diabetes mellitus patients from Kuwait. Check out the full text and abstract below.

Abstract

Background: Type 2 diabetes mellitus (T2DM) and obesity are prevalent in Kuwait. Vitamin D (VD) deficiency and leptin resistance are risk factors for both disorders. A correlation between the two risk factors has been suggested albeit inconsistently reported. Our objective was to determine the effect and association of VD and leptin levels and their related common variants with T2DM.\

Methods: This case-control study included 203 Kuwaiti T2DM patients and 162 healthy Kuwaiti controls. Leptin and VD levels were measured using enzyme linked immunosorbent assays. Genotyping of LEP rs7799039, LEPR rs1137101, VDRrs2228570 and rs731236 was performed using Taqman genotyping assays.

Results: Leptin levels were higher in T2DM patients than controls, but vitamin D levels did not differ. No correlation was found between the levels of the two hormones. VDR rs731236G associated with T2DM risk (Odds ratio 1.66, p=0.0008). VDR haplotype analysis revealed GG/AA, GA/AA or GG/AG to associate with T2DM risk (p=0.01) and increased risk of diabetic neuropathy (p=0.002). VDR rs2228570GG associated with leptin levels in T2DM (p=0.01). Effect of LEP rs7799039 on leptin (p=0.01) and VD levels (p=0.02) was only evident in healthy controls.

Conclusions: VDR rs731236G is associated with T2DM risk in Kuwait, and a VDR haplotype of a less active, low expressing VDR is associated with T2DM and diabetic neuropathy risk. Common variants in leptin and VD related genes appear to mediate the suggested positive correlation of both hormones however their influence is disrupted in T2DM.

Lari F., Alabduljaleel T., Mojiminiyi O., et al. Exploring the Relationship Between Vitamin D and Leptin Hormones in Type 2 Diabetes Mellitus Patients from Kuwait. J Horm Mol Biol Clin Investig. 2022; 10.1515/hmbci-2021-0091

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The Eagle Bioscience’s Free Soluble RANKL ELISA was utilized in a recent publication focusing on Skeletal Disease acquisition in Fibrous Dysplasia. Check out the full text and abstract below.

Abstract

Fibrous dysplasia (FD) is a rare mosaic disorder resulting in fractures, pain, and disability. Bone lesions appear during childhood and expand during skeletal growth. The rate at which FD lesions progress and the biochemical determinants of FD lesion formation have not been established, making it difficult to investigate and implement preventative therapies. The purpose of this study was to characterize FD lesion progression in children, and to identify clinical variables associated with progressive disease. Clinical data and imaging from an ongoing natural history study at the National Institutes of Health (NIH) were reviewed. 99m-Technetium methylene diphosphonate (99Tc-MDP) scans were used to determine Skeletal Burden Score (SBS), a validated quantitative scoring system. FD progression rate was determined by the change in the SBS in each patient per year. Thirty-one children had serial 99Tc-MDP scans, with a median age at first scan of 6 years (interquartile range [IQR] 4–8, range 2–10), and median follow-up 1.1 years (IQR 1.1–2.1, range 0.7–11.2). The median FD progression rate for the total group was 2.12 SBS units/year (IQR 0.81–2.94, range 0.05–7.81). FD progression rates were highest in children under age 8 years and declined with age (p = 0.03). Baseline disease severity was associated with subsequent disease progression (p = 0.009), with the highest FD progression rates in patients with moderate disease (baseline SBS 16–30), and lowest progression rates in those with severe disease (SBS ≥50). Serum levels of the bone formation marker osteocalcin were positively correlated with subsequent FD progression rate (p = 0.01, R = 0.58). There was no association between FD progression and baseline endocrinopathies, fractures, or surgery rates. FD lesions progress during childhood, particularly in younger children and those with moderate involvement. Osteocalcin may potentially serve as a biomarker for progressive disease. These findings may allow clinicians to investigate preventative therapies, and to identify children with FD who are candidates for early interventions. Published 2022. This article is a U.S. Government work and is in the public domain in the USA.

Szymczuk V., Taylor J., Michel Z., Sinaii N., Boyce A.M. Skeletal Disease Acquisition in Fibrous Dysplasia: Natural History and Indicators of Lesion Progression in Children. J Bone Miner Res. 10.1002/jbmr.4618

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The Eagle Bioscience’s Secretory IgA ELISA Assay was highlighted in a recent publication focusing on how transcytosis of IgA attenuates salmonella invasion in human enteroids and intestinal organoids. Check out the full text and abstract below.

Abstract

Secretory IgA (SIgA) is the most abundant antibody type in intestinal secretions where it contributes to safeguarding the epithelium from invasive pathogens like the Gram-negative bacterium, Salmonella enterica serovar Typhimurium (STm). For example, we recently reported that passive oral administration of the recombinant monoclonal SIgA antibody, Sal4, to mice promotes STm agglutination in the intestinal lumen and restricts bacterial invasion of Peyer’s patch tissues. In this report, we sought to recapitulate Sal4-mediated protection against STm in human Enteroids and human intestinal organoids (HIOs) as models to decipher the molecular mechanisms by which antibodies function in mucosal immunity in the human gastrointestinal tract. We confirm that Enteroids and HIO-derived monolayers are permissive to STm infection, dependent on HilD, the master transcriptional regulator of the SPI-I type three secretion system (T3SS). Stimulation of M-like cells in both Enteroids and HIOs by the addition of RANKL further enhanced STm invasion. The apical addition of Sal4 mouse IgA, as well as recombinant human Sal4 dimeric IgA (dIgA) and SIgA resulted a dose-dependent reduction in bacterial invasion. Moreover, basolateral application of Sal4 dIgA to Enteroid and HIO monolayers gave rise to SIgA in the apical compartment via a pathway dependent on expression of the polymeric immunoglobulin receptor (pIgR). The resulting Sal4 SIgA was sufficient to reduce STm invasion of Enteroid and HIO epithelial cell monolayers by ~20-fold. Recombinant Sal4 IgG was also transported in the Enteroid and HIOs, but to a lesser degree and via a pathway dependent on the neonatal Fc receptor (FCGRT). The models described lay the foundation for future studies into detailed mechanisms of IgA and IgG protection against STm and other pathogens.

Costello C.M., Willsey G.G., Richards A.F., et al. Transcytosis of IgA Attenuates Salmonella Invasion in Human Enteroids and Intestinal Organoids. Infect Immun. 2022; 90(6). 10.1128/iai.00041-22

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The Eagle Bioscience’s Rat KIM-1 ELISA Assay was utilized in a recent publication focusing on the dose-dependent renoprotective impact of Lactoferrin against glycerol-induced rhabdomyolysis and acute kidney injury. Check out the full text and abstract below.

Abstract

Acute kidney injury (AKI) is a clinical disorder with a serious impact on the quality of patients’ lives. Considering its increased worldwide prevalence, investigating novel therapeutic approaches for the management of AKI has been inevitable. Lactoferrin (LF), a glycoprotein belonging to the transferrin family, is known to play an important role in regulating iron homeostasis. This study aimed to evaluate the renoprotective effect of LF (30, 100, and 300 mg/kg orally) against glycerol (GLY)-induced rhabdomyolysis (RM) in rats. RM was induced by a single intramuscular injection of GLY 50% (10 mL/kg) after 24-h water deprivation in male Sprague–Dawley rats. LF administration conferred significant dose-dependent renoprotective impact against GLY-induced RM as evidenced by the decreased renal/somatic index and the significant improvement in renal functions as confirmed by the significant increase in creatinine clearance, decrease in serum creatinine and blood urea nitrogen, and improvement in albuminuria and proteinuria. Redox homeostasis was significantly restored in a dose-dependent manner as well. Moreover, serum interleukin-1β (IL-1β) was significantly decreased with a parallel significant decrease in renal NOD-like receptor family pyrin domain containing 3 (NLRP3) and thioredoxin interacting protein (TXNIP), kidney injury molecule-1 (KIM-1), caspase-3 expression, nuclear factor kappa B (NF-κB), cluster of differentiation (CD68) expression, and a significant increase in renal nuclear factor erythroid 2-related factor 2 (NRF2) expression. Ultimately, LF administration was associated with a significant amelioration of GLY-induced renal necrotic and inflammatory alterations. In conclusion, the observed dose-dependent nephroprotective effect of LF can be attributed to its modulatory impact on inflammatory/apoptotic/oxidative signaling.

Madkour A.H., Helal M.G., Said E., Salem H.A. Dose-Dependent Renoprotective Impact of Lactoferrin Against Glycerol-Induced Rhabdomyolysis and Acute Kidney Injury. Life Sciences. 2022; 302:1. 10.1016/j.lfs.2022.120646

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The Eagle Bioscience’s Polystreptavidin R Extraordinary High Biotin Binding Capacity was utilized in a recent publication. The researchers of this study were focusing on the use of an aptamer sandwich lateral flow assay (AptaFlow) for antibody-free SARS-CoV-2 detection. Check out the full text and abstract below.

Abstract

The COVID-19 pandemic is among the greatest health and socioeconomic crises in recent history. Although COVID-19 vaccines are being distributed, there remains a need for rapid testing to limit viral spread from infected individuals. We previously identified the SARS-CoV-2 spike protein N-terminal domain (NTD) binding DNA aptamer 1 (SNAP1) for detection of SARS-CoV-2 virus by aptamer–antibody sandwich enzyme-linked immunoassay (ELISA) and lateral flow assay (LFA). In this work, we identify a new aptamer that also binds at the NTD, named SARS-CoV-2 spike protein NTD-binding DNA aptamer 4 (SNAP4). SNAP4 binds with high affinity (<30 nM) for the SARS-CoV-2 spike protein, a 2-fold improvement over SNAP1. Furthermore, we utilized both SNAP1 and SNAP4 in an aptamer sandwich LFA (AptaFlow), which detected SARS-CoV-2 UV-inactivated virus at concentrations as low as 10⁶ copies/mL. AptaFlow costs <$1 per test to produce, provides results in <1 h, and detects SARS-CoV-2 at concentrations that indicate higher viral loads and a high probability of contagious transmission. AptaFlow is a potential approach for a low-cost, convenient antigen test to aid the control of the COVID-19 pandemic.

Yang L.F., Kacherovsky N., Panpradist N., et al. Aptamer Sandwhich Lateral Flow Assay (AptaFlow) for Antibody-Free SARS-CoV-2 Detection. Anal. Chem. 2022: 94:20, 7278–7285. https://doi.org/10.1021/acs.analchem.2c00554

If you have any questions about the Polystreptavidin R Extraordinary High Biotin Binding Capacity or any of our other offerings, please contact us here.

The Eagle Bioscience’s Calprotectin ELISA Assay Kit was utilized in a recent publication focusing on intestinal inflammation. The researchers were trying to determine an association between intestinal inflammation and growth in preterm infants from birth to hospital discharge. Check out the full text and abstract below.

Abstract

Objective:

The aim of the study was to assess intestinal inflammatory measures, urinary intestinal fatty acid-binding protein (IFABP), and fecal calprotectin (FC) by gestational age (GA) and postmenstrual age (PMA) and determine the association between intestinal inflammation and growth in preterm infants from birth to hospital discharge. We hypothesized that intestinal inflammation is associated with adverse growth in preterm infants.

Methods:

We assayed repeated measures of IFABP and FC in 72 hospitalized preterm infants (<34 weeks’ gestation). We calculated weight and length z scores at birth and discharge using the Fenton growth reference. Associations between mean IFABP or FC, growth z scores at discharge, and growth faltering (weight or length z score difference <−0.8 from birth to discharge) were assessed using mixed linear and logistic regression models, adjusted for intrafamilial correlation and potential confounders: GA, sex, birth zscore, race/ethnicity, and maternal age.

Results:

Mean IFABP was greater among infants born at earlier GA and decreased with increasing PMA. Mean FC did not vary by GA or PMA. Higher mean IFABP and FC were associated with lower discharge growth z scores and greater likelihood of growth faltering significant only for mean IFABP and discharge length z score (β = −0.353, 95% confidence interval [CI]: −0.704 to −0.002) and mean IFABP and length faltering (odds ratio [OR] 1.99, P = 0.018).

Conclusions:

Intestinal inflammation, measured by IFABP, was associated with lower length z scores and length faltering at discharge. Interventions to prevent intestinal inflammation may improve linear growth among preterm infants.

Thai J.D., Cherkekrzian S., Filatava E.J., et al. Intestinal Inflammation is Significantly Associatedd with Length Faltering in Preterm Infants at Neonatal Intensive Care Unit Discharge. J Pediatr Gastroenterol Nutr. 2022; 74(6):837-844. 10.1097/MPG.0000000000003455

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The Eagle Bioscience’s Mouse/Rat 25-OH Vitamin D ELISA was utilized in a recent publication focusing on the effects of exogenous progesterone on the expression of mineral regulatory molecules by ovine endometrium and placentome. Check out the full text and abstract below.

Abstract

This study aimed to determine whether the acceleration of conceptus development induced by the administration of exogenous progesterone (P4) during the preimplantation period of pregnancy alters calcium, phosphate, and vitamin D signaling at the maternal–conceptus interface. Suffolk ewes (n = 48) were mated to fertile rams and received daily intramuscular injections of either corn oil (CO) vehicle or 25 mg of progesterone in CO (P4) for the first 8 days of pregnancy and hysterectomized on either Day 9 (CO, n = 5; P4, n = 6), 12 (CO, n = 9; P4, n = 4) or 125 (CO, n = 14; P4, n = 10) of gestation. The expression of S100A12(P < 0.05) and fibroblast growth factor receptor (FGFR2) (P < 0.01) messenger RNAs (mRNAs) was lower in endometria from P4-treated ewes on Day 12. The expression of ADAM10 (P < 0.05) mRNA was greater in endometria from P4-treated ewes on Day 125. The expression of ADAM10 (P < 0.01), FGFR2 (P < 0.05), solute carrier (SLC)20A1 (P < 0.05), TRPV5 (P < 0.05), and TRPV6 (P < 0.01) mRNAs was greater, but KL mRNA expression was lower (P < 0.05) in placentomes from P4-treated ewes at Day 125. There was lower endometrial and greater placentomal expression of mRNAs involved in mineral metabolism and transport in twin compared to singleton pregnancies. Further, the expression of mRNAs involved in mineral metabolism and transport was greater in P4-treated twin placentomes. KL, FGF23, vitamin D receptor (VDR), S100A9, S100A12, S100G, and CYP27B1 proteins were immunolocalized in endometria and placentomes. Exogenous P4 in early pregnancy altered the expression of regulators of calcium, phosphate, and vitamin D on Day 125 of pregnancy indicating a novel effect of P4 on mineral transport at the maternal–conceptus interface.

Stenhouse C., Halloran K.M., Hoskins E.C., et al. Effects of exogenous progesterone on the expression of mineral regulatory molecules by ovine endometrium and placentomes. Biol. Reprod. 2022 https://doi.org/10.1093/biolre/ioac042

If you have any questions about the Mouse/Rat 25-OH Vitamin D ELISA or our other offerings, please contact us here.

The Eagle Bioscience’s IL-6 ELISA Assay Kit was utilized in a recent publication that focused on evaluating the antifibrotic effect of anti-CXCR4 i-body AD-114 in kidney fibrosis and elucidating the possible underlying mechanisms by utilizing the in vivo toxin-induced FA nephropathy model of CKD and the in vitro human PTC line. Check out the full-text article and abstract below.

Abstract

The G protein–coupled CXC chemokine receptor 4 (CXCR4) is a candidate therapeutic target for tissue fibrosis. A fully human single-domain antibody-like scaffold i-body AD-114-PA600 (AD-114) with specific high binding affinity to CXCR4 has been developed. To define its renoprotective role, AD-114 was administrated in a mouse model of renal fibrosis induced by folic acid (FA). Increased extracellular matrix (ECM) accumulation, macrophage infiltration, inflammatory response, TGF-β1 expression, and fibroblast activation were observed in kidneys of mice with FA-induced nephropathy. These markers were normalized or partially reversed by AD-114 treatment. In vitro studies demonstrated AD-114 blocked TGF-β1–induced upregulated expression of ECM, matrix metalloproteinase-2, and downstream p38 mitogen-activated protein kinase (p38 MAPK) and PI3K/AKT/mTOR signaling pathways in a renal proximal tubular cell line. Additionally, these renoprotective effects were validated in a second model of unilateral ureteral obstruction using a second generation of AD-114 (Fc-fused AD-114, also named AD-214). Collectively, these results suggest a renoprotective role of AD-114 as it inhibited the chemotactic function of CXCR4 as well as blocked CXCR4 downstream p38 MAPK and PI3K/AKT/mTOR signaling, which establish a therapeutic strategy for AD-114 targeting CXCR4 to limit renal fibrosis.

Cao Q., Huang C., Yi H., et al. A single-domain i-body, AD-114, attenuates renal fibrosis through blockade of CXCR4. JCI Insight. (2022) 7:4. https://doi.org/10.1172/jci.insight.143018.

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The Eagle Bioscience’s Mouse/Rat Dopamine ELISA was utilized in a recent publication focusing on the beneficial consequences of probiotic on mitochondrial hippocampus in Alzheimer’s disease. Check out the full text and abstract below.

Background

Abstract
Alzheimer’s (AD) is one of the most common neurodegenerative diseases, causing dementia and brain cells death. This study aimed to assess the ameliorating effect of Acidophilus probiotic against AD induced in rats by d-galactose and AlCl3 injection via evaluating mitochondrial parameter changes in hippocampus.

Methods
This study was carried out on rats were classified into five groups; G1 (control group), G2 (probiotic group), G3 (AD group), G4 (co-treated group) and G5 (post-treated group). By the end of the experiment, some different neurotransmitters, oxidative stress biomarkers, zinc, blood glucose, Na+K−ATPase subunit alpha 1 (ATP1A1), and gene expression of mitochondrial membrane potential (MMP) were measured.

Results
Significant changes in neurotransmitters, antioxidants levels and decreased ATP1A1 activity and gene expression of MMP in the hippocampus in G3 were detected if compared to control. Best improvement in G5 than G4 group was observed. These results were confirmed by histological and immunohistochemical studies in hippocampus.

Conclusions
Acidophilus probiotic was able to alleviate learning and memory associated injuries in AD by reducing mitochondrial dysfunction induced by d-galactose and AlCl3. This may be associated with its antioxidant properties.

Beltagy, D., Nawar, N., Mohamed, T., et al. Beneficial consequences of probiotic on mitochondrial hippocampus in Alzheimer’s disease. Journal of Complementary and Integrative Medicine, (2021).

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