Category: Publication Spotlight

A recent study utilized the Total Complement Functional Screen ELISA from Svar Life Sciences! Check out the abstract and full text below.

Abstract

Reservoir host associations have been observed among and within Borrelia genospecies, and host complement-mediated killing is a major determinant in these interactions. In North America, only a subset of Borrelia burgdorferi lineages cause the majority of disseminated infections in humans. We hypothesize that differential resistance to human complement-mediated killing may be a major phenotypic determinant of whether a lineage can establish systemic infection. As a corollary, we hypothesize that borreliacidal action may differ among human subjects. To test these hypotheses, we isolated primary B. burgdorferi clones from field-collected ticks and determined whether the killing effects of human serum differed among those clones in vitro and/or whether these effects were consistent among human sera. Clones associated with human invasiveness did not show higher survival in human serum compared to noninvasive clones. These results indicate that differential complement-mediated killing of B. burgdorferi lineages is not a determinant of invasiveness in humans. Only one significant difference in the survivorship of individual clones incubated in different human sera was detected, suggesting that complement-mediated killing of B. burgdorferi is usually similar among humans. Mechanisms other than differential human complement-mediated killing of B. burgdorferi lineages likely explain why only certain lineages cause the majority of disseminated human infections.

Pearson, P.; Rich, C.; Siegel, E.L.; Brisson, D.; Rich, S.M. Differential Resistance of Borrelia burgdorferi Clones to Human Serum-Mediated Killing Does Not Correspond to Their Predicted Invasiveness. Pathogens 2023, 12, 1238. https://doi.org/10.3390/pathogens12101238

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Eagle Bioscience’s GLP-2 ELISA Assay Kit was highlighted in recent publication! The scientists in this study induced the physiological secretion of GLP-2 via nanoparticles to help them develop a combination therapy for inflammatory bowel disease (IBD). Check out the abstract and full article below.

Abstract

Current treatments for inflammatory bowel disease (IBD) treatment consist of anti-inflammatory products. In this study, we sought to induce the physiological secretion of glucagon-like peptide 2, a peptide with intestinal growth-promoting activity, via nanoparticles while simultaneously providing with immunomodulation by tailoring the nanoparticle surface. To this end, we developed hybrid lipid hyaluronate-KPV conjugated nanoparticles loaded with teduglutide for combination therapy in IBD. The nanocarriers induced (or did not induce) immunosuppression depending on the presence (or absence) of a hyaluronan-KPV functionalization. This strategy holds promise as a nanoparticle platform for combined mucosal healing and immunomodulation in IBD treatment.

V. Marotti, et al. A nanoparticle platform for combined mucosal healing and immunomodulation in inflammatory bowel disease treatment, Bioactive Materials, Volume 32, 2024, Pages 206-221, ISSN 2452-199X, https://doi.org/10.1016/j.bioactmat.2023.09.014.

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The Eagle Bioscience’s Calprotectin ELISA Assay Kit was utilized in a recent study! This study investigated whether microbiome profiles can indidcate stress reactivity in ulcerative colitis. Check out the abstract and full text below!

Abstract

Background: Stress reactivity (SR) is associated with increased risk of flares in ulcerative colitis (UC) patients. Because both preclinical and clinical data support that stress can influence gut microbiome composition and function, we investigated whether microbiome profiles of SR exist in UC.

Methods: Ninety-one UC subjects in clinical and biochemical remission were classified into high and low SR groups by questionnaires. Baseline and longitudinal characterization of the intestinal microbiome was performed by 16S rRNA gene sequencing and fecal and plasma global untargeted metabolomics. Microbe, fecal metabolite, and plasma metabolite abundances were analyzed separately to create random forest classifiers for high SR and biomarker-derived SR scores.

Results: High SR reactivity was characterized by altered abundance of fecal microbes, primarily in the Ruminococcaceae and Lachnospiraceae families; fecal metabolites including reduced levels of monoacylglycerols (endocannabinoid-related) and bile acids; and plasma metabolites including increased 4-ethyl phenyl sulfate, 1-arachidonoylglycerol (endocannabinoid), and sphingomyelin. Classifiers generated from baseline microbe, fecal metabolite, and plasma metabolite abundance distinguished high vs low SR with area under the receiver operating characteristic curve of 0.81, 0.83, and 0.91, respectively. Stress reactivity scores derived from these classifiers were significantly associated with flare risk during 6 to 24 months of follow-up, with odds ratios of 3.8, 4.1, and 4.9. Clinical flare and intestinal inflammation did not alter fecal microbial abundances but attenuated fecal and plasma metabolite differences between high and low SR.

Conclusions: High SR in UC is characterized by microbial signatures that predict clinical flare risk, suggesting that the microbiome may contribute to stress-induced UC flares.

Jonathan P Jacobs, Jenny S Sauk, Aaron I Ahdoot, Fengting Liang, William Katzka, Hyo Jin Ryu, Ariela Khandadash, Venu Lagishetty, Jennifer S Labus, Bruce D Naliboff, Emeran A Mayer, Microbial and Metabolite Signatures of Stress Reactivity in Ulcerative Colitis Patients in Clinical Remission Predict Clinical Flare Risk, Inflammatory Bowel Diseases, 2023;, izad185, https://doi.org/10.1093/ibd/izad185

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The Eagle Bioscience’s Glutathione Total Assay Kit and Malondialdehyde HPLC Assay Kit were highlighted in a recent study! The study was conduct to examine the shielding influence of cinnamic acid against lung fibrosis induced by methotrexate. Check out the abstract and full article below!

Abstract

Purpose: Lung fibrosis is a heterogeneous lung condition characterized by excessive accumulation of scarred tissue, leading to lung architecture destruction and restricted ventilation. The current work was conducted to examine the probable shielding influence of cinnamic acid against lung fibrosis induced by methotrexate.

Methods: Rats were pre-treated with oral administration of cinnamic acid (50 mg/kg/day) for 14 days, whereas methotrexate (14 mg/kg) was orally given on the 5th and 12th days of the experiment. Pirfenidone (50 mg/kg/day) was used as a standard drug. At the end of the experiment, oxidative parameters (malondialdehyde, myeloperoxidase, nitric oxide, and total glutathione) and inflammatory mediators (tumor necrosis factor-α and interleukin-8), as well as transforming growth factor-β and collagen content, as fibrosis indicators, were measured in lung tissue.

Results: Our results revealed that cinnamic acid, as pirfenidone, effectively prevented the methotrexate-induced overt histopathological damage. This was associated with parallel improvements in oxidative, inflammatory, and fibrotic parameters measured. The outcomes of cinnamic acid administration were more or less the same as those of pirfenidone. In conclusion, pre-treatment with cinnamic acid protects against methotrexate-induced fibrosis, making it a promising prophylactic adjuvant therapy to methotrexate and protecting against its possible induction of lung fibrosis.

Abdalhameid, E., Abd El-Haleim, E.A., Abdelsalam, R.M. et al. Cinnamic acid mitigates methotrexate-induced lung fibrosis in rats: comparative study with pirfenidone. Naunyn-Schmiedeberg’s Arch Pharmacol (2023). https://doi.org/10.1007/s00210-023-02652-w

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The Eagle Bioscience’s Secretory IgA ELISA Assay Kit was highlighted in a recent publication! This study conducted a double-blind randomized trial to help determine if synbiotic supplementation is effective in healthy adults. Check out the abstract and full text below.

Abstract

Synbiotics are increasingly used by the general population to boost immunity. However, there is limited evidence concerning the immunomodulatory effects of synbiotics in healthy individuals. Therefore, we conducted a double-blind, randomized, placebo-controlled study in 106 healthy adults. Participants were randomly assigned to receive either synbiotics (containing Bifidobacterium lactis HN019 1.5 × 108 CFU/d, Lactobacillus rhamnosus HN001 7.5 × 107 CFU/d, and fructooligosaccharide 500 mg/d) or placebo for 8 weeks. Immune parameters and gut microbiota composition were measured at baseline, mid, and end of the study. Compared to the placebo group, participants receiving synbiotic supplementation exhibited greater reductions in plasma C-reactive protein (P = 0.088) and interferon-gamma (P = 0.008), along with larger increases in plasma interleukin (IL)-10 (P = 0.008) and stool secretory IgA (sIgA) (P = 0.014). Additionally, synbiotic supplementation led to an enrichment of beneficial bacteria (Clostridium_sensu_stricto_1, Lactobacillus, Bifidobacterium, and Collinsella) and several functional pathways related to amino acids and short-chain fatty acids biosynthesis, whereas reduced potential pro-inflammatory Parabacteroides compared to baseline. Importantly, alternations in anti-inflammatory markers (IL-10 and sIgA) were significantly correlated with microbial variations triggered by synbiotic supplementation. Stratification of participants into two enterotypes based on pre-treatment Prevotella-to-Bacteroides (P/B) ratio revealed a more favorable effect of synbiotic supplements in individuals with a higher P/B ratio. In conclusion, this study suggested the beneficial effects of synbiotic supplementation on immune parameters, which were correlated with synbiotics-induced microbial changes and modified by microbial enterotypes. These findings provided direct evidence supporting the personalized supplementation of synbiotics for immunomodulation.

Xiaoqin Li, Shan Hu, Jiawei Yin, Xiaobo Peng, Lei King, Linyan Li, Zihui Xu, Li Zhou, Zhao Peng, Xiaolei Ze, Xuguang Zhang, Qiangchuan Hou, Zhilei Shan & Liegang Liu (2023) Effect of synbiotic supplementation on immune parameters and gut microbiota in healthy adults: a double-blind randomized controlled trial, Gut Microbes, 15:2, DOI: 10.1080/19490976.2023.2247025

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The Eagle Bioscience’s Folic Acid ELISA Assay Kit Highlighted in a recent study! The study was conducted to assess the disruption in nutritional attributes of Capsicum annuum by five different microplastic (MP) types. Check out the abstract and full text below.

Abstract

This study was executed to assess the disruption in nutritional attributes of Capsicum annuum by five different microplastic (MP) types i.e. polyvinylchloride (PVC), polystyrene (PS), high-density polyethylene (HDPE), low-density polyethylene (LDPE), and polyethylene terephthalate (PET). Significant (P ≤ 0.05) differences were recorded among traits of C. annuum fruit concerning the type of MPs. PVC was more hazardous than the other MPs and depleted maximum protein content. Likewise, HDPE exerted a 51.62% reduction in carbohydrates compared to the control. Vitamin-A (-32.09%) and vitamin-B6 (-37%) were severely influenced by the PVC in C. annuum fruit. HDPE and PVC both declined the oleic acid contents. PVC caused a 47.6% reduction in linoleic acid while the least damaging was the PET (4.71%) for this attribute. Palmitic acid and stearic acid were however more negatively affected by the HDPE. The PVC and HDPE severely degraded the total flavonoid contents and phenolics. Macro and micronutrients of C. annuum fruit were also negatively influenced by all the five MPs used in this study. HDPE, PVC and LDPE, respectively caused significant repression in Ca, K, Mg and Zn (P ≤ 0.05). Overall, HDPE and PVC caused significant damage and decreased nutritional contents. This is, so far, the premier study unraveling the changes in the nutrition of C. annuum fruits due to MPs. Accordingly, further research is highly recommended on the changes caused by MPs in the nutritional value of food crops.

Khadiga Alharbi, Muhammad Aqeel, Noreen Khalid, Atia Nazir, Muhammad Kashif Irshad, Fahad Mohammed Alzuaibr, Haifa AbdulAziz Sakit AlHaithloul, Noreen Akhter, Omar Mahmoud Al-Zoubi, Muhammad Qasim, Khalid M.Al Syaad, Manal Abdullah AlShaqhaa, Ali Noman. Microplastics in soil differentially interfere with nutritional aspects of chilli peppers. South African Journal of Botany. Volume 160. 2023. Pages 402-413. ISSN 0254-6299, https://doi.org/10.1016/j.sajb.2023.07.027.

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The Eagle Bioscience’s Dopamine ELISA Assay Kit was utilized in a recent publications! The aim of the study was to investigate the potential of iron oxide nanoparticles produced using ascorbic acid (AA-IONPs) against Parkinson’s Disease. Check out the abstract and full text below!

Abstract

One of the most prevalent neurological movement diseases affecting the geriatric population globally is Parkinson’s disease (PD). Recent studies have highlighted the potency of biomolecules in the generation of nanomaterials and also over their impact on neuroprotection. The objective of this research was to investigate the potential of iron oxide nanoparticles produced using ascorbic acid (AA-IONPs) against PD. Numerous analytical methods including UV–Vis analysis, Fourier-Transform Infrared Spectroscopy (FTIR), dynamic light scattering (DLS), and electron microscopy (SEM, TEM), were used to analyze the produced AA-IONPs. Nitric oxide, prostaglandin E2, and inflammatory cytokines analyses such as IL-6 and IL-1 were employed to assess the neuroprotective effect of synthesized AA-IONPs on inflammatory agent lipopolysaccharides driven murine microglial BV2 cells. And also Parkinson-induced C57BL/6 mice were given the nanoparticle treatment to confirm the in vivo effects of the produced nanoparticles. Our characterization findings had demonstrated that AA-IONPs have a significant role in acting as an ideal nano drug and may have the ability to reduce inflammation in in vitro murine microglial BV2. The outcomes of in vivo tests conclusively show that AA-IONPs had reduced neuroinflammation and enhanced motor coordination in Parkinson’s disease-induced rats.

Li, L., Luo, P., Wu, S. et al. Deciphering the neuroprotective effect of ascorbic acid mediated synthesis of iron oxide nanoparticles against Parkinson’s disease: an in vitro and in vivo approach. Macromol. Res. 31, 949–960 (2023). https://doi.org/10.1007/s13233-023-00186-x

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The Biomedica Human IL-6 High Sensitive ELISA Assay Kit was highlighted in a recent publication that explored factors associated with incident vertebral fractures in glucocorticoid-treated Duchenne muscular dystrophy. Check out the abstract and full text below!

Abstract

Purpose: Prevention of fractures is an unmet need in glucocorticoid (GC)-treated Duchenne muscular dystrophy. This study explored factors associated with incident vertebral fractures (VFs) to inform future fracture prevention efforts.

Methods: VFs were evaluated prospectively at study baseline and 12 months on lateral spine radiographs in participants aged 4 to 25 years with Duchenne muscular dystrophy. Clinical factors were analyzed for their association with the change in Spinal Deformity Index (sum of the Genant-defined VF grades from T4 to L4) between baseline and 12 months.

Results: Thirty-eight males were evaluated (mean ± SD age at baseline 11.0 ± 3.6 years; mean ± SD GC duration at baseline 4.1 ± 3.1 years; 74% ambulatory). Nine of 38 participants (24%) had 17 incident VFs, of which 3/17 VFs (18%) were moderate/severe. Participants with 12-month incident VF had lower mean ± SD baseline lumbar spine areal bone mineral density Z-scores (-2.9 ± 1.0 vs -1.9 ± 1.1; P = .049) and lower total body less head areal bone mineral density Z-scores (-3.1 ± 1.2 vs -1.6 ± 1.7; P = .036). Multivariable linear regression showed that at least 1 VF at baseline (P < .001), a higher number of antecedent non-VF (P < .001), and greater bone age delay at baseline (P = .027) were significant predictors of an increase in the Spinal Deformity Index from baseline to 12 months.

Conclusion: The observation that ≥ 1 prevalent VF and/or non-VF were the strongest predictors of incident VFs at 12 months supports the need for prevention of first fractures in this high-risk setting. Bone age delay, a marker of GC exposure, may assist in the prioritization of patients in efforts to prevent first fractures.

Keywords: Duchenne muscular dystrophy; bone fragility; glucocorticoids; incident fractures; osteoporosis; vertebral fractures.

Risk Factors Associated with Incident Vertebral Fractures in Steroid-treated Males with Duchenne Muscular Dystrophy . Phung K, McAdam L, Ma J, McMillan HJ, Jackowski S, Scharke M, Matzinger MA, Shenouda N, Koujok K, Jaremko JL, Wilson N, Walker S, Hartigan C, Khan N, Page M, Robinson ME, Saleh DS, Smit K, Rauch F, Siminoski K, Ward LMJ Clin Endocrinol Metab. 2023 Aug 23:dgad435. doi: 10.1210/clinem/dgad435. Epub ahead of print.PMID: 37610420

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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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