Author: Eagle Biosciences

Frailty is a syndrome characterized by the gradual decline in physical function, strength, and endurance, typically associated with aging. Frailty increases the risk of falls, fractures, disability, and death, making early detection and intervention critical. The onset of frailty is often subtle and difficult to identify in its early stages, which is why there is increasing interest in finding reliable biomarkers for its detection.

Sclerostin has emerged as a potential biomarker for the early detection of frailty due to its involvement in both bone metabolism and muscle function. Studies suggest that changes in sclerostin levels are associated with age-related declines in skeletal muscle mass, strength, and function — all of which are central components of frailty.

Biomedica’s Sclerostin ELISA Kit was used in a first time study that explored the association between circulating sclerostin levels and frailty. Click below for the full publication, where you can find the abstract and key findings!

Baek, Ji Yeon, et al. “Elevated circulating Sclerostin levels in frail older adults: Implications beyond bone health.” Endocrinology and Metabolism, vol. 40, no. 1, 28 Feb. 2025, pp. 73–81, https://doi.org/10.3803/enm.2024.2100.

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The BI-CAT Adrenaline & Noradrenaline ELISA Assay Kit was utilized in a recent study that focused on if low-dose glucagon is needed and effective in preventing fasted exercise-induced hypoglycaemia in type 1 diabetes. Check out the abstract and full text details below!

Abstract

Aim: The aim of this study is to evaluate and compare the plasma glucose (PG) response during spontaneous fasted morning moderate-intensity exercise with and without injection of subcutaneous glucagon in adults with type 1 diabetes (T1D) treated with an automated insulin delivery (AID) system.

Methods:
Ten adults (four female) with T1D (age 50 [42–67] years, diabetes duration: 22 [14–44] years, HbA1c: 55 [47–69] mmol/mol) treated with the MiniMed™ 780G AID system participated in a proof-of-concept two-period, crossover trial. Fasting participants undertook a 45 min bout of continuous moderate-intensity (~60% V̇O_2peak) exercise on a cycle ergometer followed by 1 h of rest. Before exercise, 150-μg glucagon was administered subcutaneously on visit 1 (GLUC) but not on visit 2 (NO-GLUC). Temporary target on the AID was activated 15 min before until 15 min after exercise cessation. Blood samples were taken at 5- and 15-min intervals for measuring PG and biomarkers. Data were analysed using paired t tests or repeated measures ANOVA.

Results
Time in range (3.9–10.0 mmol/L) was 100% on both study visits. No hypoglycaemia (<3.9 mmol/L) occurred in either arm. The GLUC arm had significantly higher mean PG (p = 0.01), area under the PG curve (p = 0.01), coefficient of variation (p < 0.01), peak PG (p = 0.01) and PG at the end of exercise (p < 0.01). No differences in endogenous gluco-regulatory hormones were observed between visits.

Conclusion
Adults with T1D treated with the MiniMed™ 780G can perform spontaneous fasted moderate-intensity exercise without hypoglycaemia. Therefore, glucagon was not needed for prevention of hypoglycaemia in such situations.

Lundemose, Sissel Banner, et al. “Is low‐dose glucagon needed and effective in preventing fasted exercise‐induced hypoglycaemia in type 1 diabetes treated with the minimed 780g, an automated insulin delivery system?” Diabetes, Obesity and Metabolism, 27 Nov. 2024, https://doi.org/10.1111/dom.16103.

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The Mouse Albumin ELISA Assay Kit was utilized in a recent study! The study demonstrates the beneficial role of early immune activation during stress, revealing that the immune system could protect against psychological insults. Access the abstract and full text below.

Abstract

Psychological stress and its sequelae pose a major challenge to public health. Immune activation is conventionally thought to aggravate stress-related mental diseases such as anxiety disorders and depression. Here, we sought to identify potentially beneficial consequences of immune activation in response to stress. We showed that stress led to increased interleukin (IL)-22 production in the intestine as a result of stress-induced gut leakage. IL-22 was both necessary and sufficient to attenuate stress-induced anxiety behaviors in mice. More specifically, IL-22 gained access to the septal area of the brain and directly suppressed neuron activation. Furthermore, human patients with clinical depression displayed reduced IL-22 levels, and exogenous IL-22 treatment ameliorated depressive-like behavior elicited by chronic stress in mice. Our study thus identifies a gut-brain axis in response to stress, whereby IL-22 reduces neuronal activation and concomitant anxiety behavior, suggesting that early immune activation can provide protection against psychological stress.

Xia, Mengyu, et al. “Elevated IL-22 as a result of stress-induced gut leakage suppresses septal neuron activation to ameliorate anxiety-like behavior.” Immunity, vol. 58, no. 1, Jan. 2025, https://doi.org/10.1016/j.immuni.2024.11.008.

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The L-Ornithine ELISA Assay Kit was utilized in a recent study! The study shows the benefits of combined liver and retinal OAT supplementation for the treatment of GACR. For more details, reference the abstract and access to the full text below.

Abstract

Gyrate atrophy of the choroid and retina (GACR) is due to ornithine aminotransferase (OAT) deficiency, which causes hyperornithinemia, leading to retinal pigment epithelium, followed by choroidal and retinal degeneration. Adeno-associated virus serotype 8 (AAV8) vector-mediated OAT (AAV8-OAT) liver gene transfer reduces ornithinemia in the Oat^−/− mouse model of GACR and improves retinal function and structure. Since OAT is expressed in various tissues including the retina, we investigated the efficacy of restoration of OAT expression in either retina or liver or both tissues on the retinal phenotype of Oat^−/− mice. Intravenous and subretinal administration of AAV8-OAT resulted in intraocular and liver OAT expression with reduced ornithinemia after intravenous AAV8-OAT administration, while intraocular ornithine levels were significantly reduced only following combined gene delivery. Accordingly, only Oat^−/− animals treated with combined intravenous and subretinal AAV8-OAT administrations showed significant improvements in both retinal morphology and function. This work shows the benefits of combined liver and retinal OAT supplementation for the treatment of GACR.

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We’re excited to announce that the Noradrenaline (Norepinephrine) Sensitive ELISA was featured in a recent publication! Check out access the abstract and full text below.

Abstract

Spinal cord injury triggers leukocyte mobilization from the peripheral circulation to the injury site, exacerbating spinal cord damage. Simultaneously, bone marrow hematopoietic stem cells (HSCs) and splenic leukocytes rapidly mobilize to replenish the depleted peripheral blood leukocyte pool. However, current treatments for spinal cord injuries overlook interventions targeting peripheral immune organs and tissues, highlighting the need to develop novel drugs capable of effectively regulating peripheral immunity and treating spinal cord injuries. In this study, we designed, synthesized, and characterized novel Ejiao carbon dots (EJCDs) that inhibit myeloid cell proliferation and peripheral migration by promoting HSC self-renewal, and distinct differentiation into erythroid progenitors in vitro and in vivo. Additionally, EJCDs attenuate the immune response in the spleen, leukocytes’ reservoir, following spinal cord injury by diminishing the local infiltration of monocytes and macrophages while promoting motor function recovery. These effects are mediated through the downregulation of CCAAT enhancer binding protein-β expression in the spleen and the upregulation of FZD4 protein expression in Lin⁻ Sca-1⁺ c-kit⁺ cells (LSKs) within the bone marrow. Our findings demonstrate that EJCDs effectively reduce myeloid cell infiltration post-spinal cord injury and promote neurological recovery, making them promising therapeutic candidates for treating spinal cord injuries.

Li, Junjin, et al. “Novel carbon dots with dual modulatory effects on the bone marrow and spleen as a potential therapeutic candidate for treating spinal cord injury.” Bioactive Materials, vol. 45, Mar. 2025, pp. 534–550, https://doi.org/10.1016/j.bioactmat.2024.11.032.

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The Eagle Bioscience’s Noradrenaline ( Norepinephrine) High Sensitive ELISA was utilized in a recent publication that focused on how β₁-adrenergic receptor links sympathetic nerves to T cell exhaustion. Check out the full text and abstract below!

Abstract

CD8⁺ T cells are essential components of the immune response against viral infections and tumors, and are capable of eliminating infected and cancerous cells. However, when the antigen cannot be cleared, T cells enter a state known as exhaustion¹. Although it is clear that chronic antigen contributes to CD8⁺ T cell exhaustion, less is known about how stress responses in tissues regulate T cell function. Here we show a new link between the stress-associated catecholamines and the progression of T cell exhaustion through the β₁-adrenergic receptor ADRB1. We identify that exhausted CD8⁺ T cells increase ADRB1 expression and that exposure of ADRB1⁺ T cells to catecholamines suppresses their cytokine production and proliferation. Exhausted CD8⁺ T cells cluster around sympathetic nerves in an ADRB1-dependent manner. Ablation of β₁-adrenergic signaling limits the progression of T cells towards the exhausted state in chronic infection and improves effector functions when combined with immune checkpoint blockade (ICB) in melanoma. In a pancreatic cancer model resistant to ICB, β-blockers and ICB synergize to boost CD8⁺ T cell responses and induce the development of tissue-resident memory-like T cells. Malignant disease is associated with increased catecholamine levels in patients^2,3, and our results establish a connection between the sympathetic stress response, tissue innervation and T cell exhaustion. Here, we uncover a new mechanism by which blocking β-adrenergic signaling in CD8⁺ T cells rejuvenates anti-tumor functions.

Globig, AM., Zhao, S., Roginsky, J. et al. The β₁-adrenergic receptor links sympathetic nerves to T cell exhaustion. Nature 622, 383-392 (2023).

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The Eagle Bioscience’s easYmer H2-Db MHC Tetramer was highlighted in a recent publication that focused on killing tumor-associated bacteria with a liposomal antibiotic and how it generates neoantigens that induce anti-tumor immune responses. Check out the full text and abstract below!

Abstract

Increasing evidence implicates the tumor microbiota as a factor that can influence cancer progression. In patients with colorectal cancer (CRC), we found that pre-resection antibiotics targeting anaerobic bacteria substantially improved disease-free survival by 25.5%. For mouse studies, we designed an antibiotic silver-tinidazole complex encapsulated in liposomes (LipoAgTNZ) to eliminate tumor-associated bacteria in the primary tumor and liver metastases without causing gut microbiome dysbiosis. Mouse CRC models colonized by tumor-promoting bacteria (Fusobacterium nucleatum spp.) or probiotics (Escherichia coliNissle spp.) responded to LipoAgTNZ therapy, which enabled more than 70% long-term survival in two F. nucleatum-infected CRC models. The antibiotic treatment generated microbial neoantigens that elicited anti-tumor CD8⁺ T cells. Heterologous and homologous bacterial epitopes contributed to the immunogenicity, priming T cells to recognize both infected and uninfected tumors. Our strategy targets tumor-associated bacteria to elicit anti-tumoral immunity, paving the way for microbiome–immunotherapy interventions.

Wang, M., Rousseau, B., Qiu, K. et al. Killing tumor-associated bacteria with a liposomal antibiotic generates neoantigens that induce anti-tumor immune responses. Nat Biotechnol (2023).

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The Eagle Bioscience’s Calprotectin ELISA Assay Kit was utilized in a recent publication that explored intestinal microbiome and metabolome signatures in patients with chronic granulomatous disease. Check out the full text and abstract below!

Background

Chronic granulomatous disease (CGD) is caused by defects in any 1 of the 6 subunits forming the nicotinamide adenine dinucleotide phosphate oxidase complex 2 (NOX2), leading to severely reduced or absent phagocyte-derived reactive oxygen species production. Almost 50% of patients with CGD have inflammatory bowel disease (CGD-IBD). While conventional IBD therapies can treat CGD-IBD, their benefits must be weighed against the risk of infection. Understanding the impact of NOX2 defects on the intestinal microbiota may lead to the identification of novel CGD-IBD treatments.

Objective

We sought to identify microbiome and metabolome signatures that can distinguish individuals with CGD and CGD-IBD.

Methods

Results

We identified distinct intestinal microbiome and metabolome profiles in patients with CGD compared to healthy individuals. We observed enrichment for Erysipelatoclostridium spp, Sellimonas spp, and Lachnoclostridium spp in CGD stool samples. Despite differences in bacterial alpha and beta diversity between the 2 cohorts, several taxa correlated significantly between both cohorts. We further demonstrated that patients with CGD-IBD have a distinct microbiome and metabolome profile compared to patients without CGD-IBD.

Conclusion

Intestinal microbiome and metabolome signatures distinguished patients with CGD and CGD-IBD, and identified potential biomarkers and therapeutic targets.

Chandrasekaran, Prabha, et al. “Intestinal microbiome and metabolome signatures in patients with chronic granulomatous disease.” Journal of Allergy and Clinical Immunology, 2023.

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The Eagle Bioscience’s Serotonin ELISA Assay was utilized in a recent publication that explored the modification of the serotonergic systems and phenotypes by gestational micronutrients. Check out the full text and abstract below.

Abstract

Micronutrients consumed in excess or imbalanced amounts during pregnancy may increase the risk of metabolic diseases in offspring, but the mechanisms underlying these effects are unknown. Serotonin (5-hydroxytryptamine, 5-HT), a multifunctional indoleamine in the brain and the gut, may have key roles in regulating metabolism. We investigated the effects of gestational micronutrient intakes on the central and peripheral serotonergic systems as modulators of the offspring’s metabolic phenotypes. Pregnant Wistar rats were fed an AIN-93G diet with 1-fold recommended vitamins (RV), high 10-fold multivitamins (HV), high 10-fold folic acid with recommended choline (HFolRC), or high 10-fold folic acid with no choline (HFolNC). Male and female offspring were weaned to a high-fat RV diet for 12 weeks. We assessed the central function using the 5-HT_2C receptor agonist, 1-(3-chlorophenyl)piperazine (mCPP), and found that male offspring from the HV- or HFolRC-fed dams were less responsive (P < 0.05) whereas female HFolRC offspring were more responsive to mCPP (P < 0.01) at 6 weeks post-weaning. Male and female offspring from the HV and HFolNC groups, and male HFolRC offspring had greater food intake (males P < 0.001; females P < 0.001) and weight gain (males P < 0.0001; females P < 0.0001), elevated colon 5-HT (males P< 0.01; females P < 0.001) and fasting glucose concentrations (males P < 0.01; females P < 0.01), as well as body composition toward obesity (males P < 0.01; females P < 0.01) at 12 weeks post-weaning. Colon 5-HT was correlated with fasting glucose concentrations (males R²=0.78, P < 0.0001; females R²=0.71, P < 0.0001). Overall, the serotonergic systems are sensitive to the composition of gestational micronutrients, with alterations consistent with metabolic disturbances in offspring.

Chen, Vicki, et al. “Modification of the Serotonergic Systems and Phenotypes by Gestational Micronutrients.” Journal of Endocrinology, vol. 257, no. 2, 2023, https://doi.org/10.1530/joe-22-0305.

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