COVID-19 ELISA

Eagle Biosciences’ COVID-19 IgM and IgG ELISA Assay Kits were recently highlighted in a study. This study evaluated the different tools that have become available for COVID testing and research.

Abstract


Recent severe acute respiratory syndrome 2 (SARS-CoV-2) known as COVID-19, presents a deadly challenge to the global healthcare system of developing and developed countries, exposing the limitations of health facilities preparedness for emerging infectious disease pandemic. Opportune detection, confinement, and early treatment of infected cases present the first step in combating COVID-19. In this review, we elaborate on various COVID-19 diagnostic tools that are available or under investigation. Consequently, cell culture, followed by an indirect fluorescent antibody, is one of the most accurate methods for detecting SARS-CoV-2 infection. However, restrictions imposed by the regulatory authorities prevented its general use and implementation. Diagnosis via radiologic imaging and reverse transcriptase PCR assay is frequently employed, considered as standard procedures, whereas isothermal amplification methods are currently on the verge of clinical introduction. Notably, techniques such as CRISPR-Cas and microfluidics have added new dimensions to the SARS-CoV-2 diagnosis. Furthermore, commonly used immunoassays such as enzyme-linked immunosorbent assay (ELISA), lateral flow immunoassay (LFIA), neutralization assay, and the chemiluminescent assay can also be used for early detection and surveillance of SARS-CoV-2 infection. Finally, advancement in the next generation sequencing (NGS) and metagenomic analysis are smoothing the viral detection further in this global challenge.

To read more click here.

Oishee MJ, Ali T, Jahan N, et al. COVID-19 Pandemic: Review of Contemporary and Forthcoming Detection Tools. Infect Drug Resist. 2021;14:1049-1082. Published 2021 Mar 17. doi:10.2147/IDR.S289629

Related Products
Coronavirus COVID-19 IgM ELISA Assay Kit
Coronavirus COVID-19 IgG ELISA Assay Kit
COVID-19 Nucleocapsid IgG Quantitative ELISA Assay Kit
COVID-19 S-Protein Specific IgG Quantitative ELISA Assay Kit
COVID-19 Neutralizing Antibody Quantitative ELISA Assay Kit

DHEA ELISA Publication

Evidence for fasting induced extra-adrenal steroidogenesis in the male brown anole, Anolis sagrei

The Eagle Biosciences DHEA ELISA was used in a recent study testing if fasting could induce adrenal tissues to produce glucocorticoids (GCs) and dehydroepiandrosterone (DHEA) to coordinate different physiological processes.

Abstract


Glucocorticoids (GCs) and dehydroepiandrosterone (DHEA) are steroids secreted by the adrenal glands into circulation to effect distant target tissues and coordinate physiological processes. This classic systemic view of steroids has been challenged by evidence that other tissues can independently synthesize their own steroids. Little is known however regarding circumstances that can promote this extra-adrenal steroidogenesis. Here we tested if fasting can induce tissues to increase GC and DHEA synthesis in the brown anole lizard Anolis sagrei. Lizards fasted for eight days lost body mass and increased fatty acid oxidation. Fasting also increased plasma concentrations of DHEA and corticosterone, but not cortisol. Corticosterone concentration within the adrenals, heart, intestines, lungs and liver exceeded that in plasma, with the latter two increasing with fasting. Levels of DHEA in the adrenals and heart were higher than in plasma, but no significant effect of fasting was observed, expect for a noticeable increase in intestinal DHEA. Two steroidogenic genes, the steroidogenic acute regulatory (Star) protein and Cyp17a1, a cytochrome P450 enzyme, were expressed in several tissues including the liver, lungs and intestines, which were increased with fasting. Continued research should aim to test for expression of additional enzymes further along the steroidogenic pathway. Nonetheless these data document potential extra-adrenal steroidogenesis as a possible mechanism for coping with energy shortages, although much work remains to be done to determine the specific roles of locally synthesized steroids in each tissue.

To learn more and read the full publication, click here.

Related Products:

DHEA ELISA Assay Kit
DHEA-S ELISA Assay  Kit

Calprotectin ELISA

Does Human Milk Fortifier Affect Intestinal Inflammation in Preterm Infants?

Eagle Biosciences’ Calprotectin ELISA Assay Kit was used in a recent study dealing with inflammation of preterm infants in response to human milk fortifier. The Calprotectin ELISA Assay is part of our line of Gastrointestinal Assays which is a line of highly sensitive and specific kits used to detect the concentration of a variety of samples in serum, plasma, tissue, urine, and saliva.

Abstract


Background: Fecal calprotectin, a recognized marker of intestinal inflammation, is derived from neutrophil migration to a site of inflammation. Introduction of bovine-based human milk fortifier containing intact protein in preterm infants is associated with an increase in fecal calprotectin suggestive of intestinal inflammation. Newer fortifiers contain protein hydrolysates in place of intact protein.

Objective: To measure fecal calprotectin in human milk-fed preterm infants before and after human milk fortification using a fortifier containing hydrolyzed protein.

Methods: Serial stool samples were collected from 24 infants beginning at the first week to 60 days postnatal age. To compare the effect of human milk fortification, samples collected before and after fortification were compared. Infant demographics, diet, postnatal morbidities, and maternal characteristics were recorded.

Results: A total of 401 stool samples were collected from 24 study infants who had a birth weight of 993 ± 277 g (mean ± standard deviation), gestational age 27.5 ± 2.8 weeks, and fortifier initiation at 14 days. Median fecal calprotectin before and after fortification were similar. Calprotectin levels were not correlated with birth weight or gestational age but were inversely correlated with postnatal age (p = 0.005), use of fortifier (p < 0.001), receipt of antibiotics antenatally (p = 0.007) and postnatally (p = 0.008). After adjusting for postnatal age, calprotectin levels were significantly lower following receipt of fortifier (p < 0.001) and postnatal antibiotics (p < 0.001).

Conclusions: The feeding of protein hydrolysate-containing human milk fortifiers does not appear to be associated with increases in a marker of intestinal inflammation.

Click here for the full text.

Related Products

NGAL (Stool) ELISA Assay Kit
S100A8/A9 (MRP8/14, Calprotectin, Mouse/Rat) ELISA Kit
Stool Sample Collection Kit

COVID-19 IgG and IgA ELISA Feature in Recent Study Analyzing Antibody Response to SARS-CoV-2 Exposure and Symptom Onset

A study has been published in Viruses titled Persisting Neutralizing Activity to SARS-CoV-2 over Months in Sera of COVID-19 Patients by B, Flehming et al. This study takes a look at the long term presences of SARS-CoV-2 RNA and IgG and IgA antibodies in three patients diagnosed with COVID-19 over a six month period. This research utilized the COVID-19 Nucleocapsid IgG Quantitative ELISA Assay Kit and the Anti-SARS-CoV-2 IgA (S1 RBD) ELISA Assay offered by Eagle Biosciences. The results of this study indicate that immunity to the virus may persist for a couple of months after onset of symptoms. These findings are consistent with some other studies done with larger cohorts of COVID-19 patients, however similar longitudinal studies should be done in the future to corroborate these findings.

Abstract


The relationship between the nasopharyngeal virus load, IgA and IgG antibodies to both the S1-RBD-protein and the N-protein, as well as the neutralizing activity (NAbs) against SARS-CoV-2 in the blood of moderately afflicted COVID-19 patients, needs further longitudinal investigation. Several new serological methods to examine these parameters were developed, validated and applied in three patients of a family which underwent an ambulatory course of COVID-19 for six months. The virus load had almost completely disappeared after about four weeks. Serum IgA levels to the S1-RBD-protein and, to a lesser extent, to the N-protein, peaked about three weeks after clinical disease onset but declined soon thereafter. IgG levels rose continuously, reaching a plateau at approximately six weeks, and stayed elevated over the observation period. Virus-neutralizing activity reached a peak about 4 weeks after disease onset but dropped slowly. The longitudinal associations of virus neutralization and the serological immune response suggest immunity in patients even after a mild clinical course of COVID-19.

Click here for the full text.

To view Eagle Biosciences’ extensive collection of SARS-CoV-2 Assays and other products click here. 

EagleBio Endocrinology

Confirmation and Identification of Biomarkers Implicating Environmental Triggers in the Pathogenesis of Type 1 Diabetes

Frontiers in Immunology

Numerous ELISA Assay Kits from our endocrinology line were used in a recent study published out of the University of Nebraska Medical Center in Omaha, Nebraska. These kits were used to analyze blood plasma for biomarkers that could implicate environmental triggers for the pathogenesis of Type 1 Diabetes. These kits included;

Anti-GAD ELISA Assay Kit

Anti-IA2 ELISA Assay Kit

Anti-tTG IgA ELISA Assay Kit

High Sensitive Anti-TPO ELISA Assay Kit

Abstract


Multiple environmental triggers have been proposed to explain the increased incidence of type 1 diabetes (T1D). These include viral infections, microbiome disturbances, metabolic disorders, and vitamin D deficiency. Here, we used ELISA to examine blood plasma from juvenile T1D subjects and age-matched controls for the abundance of several circulating factors relevant to these hypotheses. We screened plasma for sCD14, mannose binding lectin (MBL), lipopolysaccharide binding protein (LBP), c-reactive protein (CRP), fatty acid binding protein 2 (FABP2), human growth hormone, leptin, total adiponectin, high molecular weight (HMW) adiponectin, total IgG, total IgA, total IgM, endotoxin core antibodies (EndoCAbs), 25(OH) vitamin D, vitamin D binding protein, IL-7, IL-10, IFN-γ, TNF-α, IL-17A, IL-18, and IL-18BPa. Subjects also were tested for prevalence of antibodies targeting adenovirus, parainfluenza 1/2/3, Coxsackievirus, cytomegalovirus, Epstein-Barr virus viral capsid antigen (EBV VCA), herpes simplex virus 1, and Saccharomyces cerevisiae. Finally, all subjects were screened for presence and abundance of autoantibodies targeting islet cell cytoplasmic proteins (ICA), glutamate decarboxylase 2 (GAD65), zinc transporter 8 (ZNT8), insulinoma antigen 2 (IA-2), tissue transglutaminase, and thyroid peroxidase, while β cell function was gauged by measuring c-peptide levels. We observed few differences between control and T1D subjects. Of these, we found elevated sCD14, IL-18BPa, and FABP2, and reduced total IgM. Female T1D subjects were notably elevated in CRP levels compared to control, while males were similar. T1D subjects also had significantly lower prevalence of EBV VCA antibodies compared to control. Lastly, we observed that c-peptide levels were significantly correlated with leptin levels among controls, but this relationship was not significant among T1D subjects. Alternatively, adiponectin levels were significantly correlated with c-peptide levels among T1D subjects, while controls showed no relationship between these two factors. Among T1D subjects, the highest c-peptide levels were associated with the lowest adiponectin levels, an indication of insulin resistance. In total, from our examination we found limited data that strongly support any of the hypotheses investigated. Rather, we observed an indication of unexplained monocyte/macrophage activation in T1D subjects judging from elevated levels of sCD14 and IL-18BPa. These observations were partnered with unique associations between adipokines and c-peptide levels among T1D subjects.

To learn more and read the full publication, click here.

For a full list of Eagle Bioscience’s Endocrinology line of ELISA kits click here.

A new article published by Nelly Kanberg, et al. titled Neurochemical evidence of astrocytic and neuronal injury commonly found in COVID-19 has set out to study how COVID-19 impacts the central nervous system. It’s already known how this novel coronavirus effects the respiratory system, but does the body’s inflammatory response to this virus cause lasting effects to the nervous system?

For this study, two biomarkers in human plasma were measured; neurofilament light chain protein (NfL) and glial fibrillary acidic protein (GFAP). The samples came from patients who had mild, moderate or severe cases of COVID-19 (n=47). Of those 47 patients, the ones who had a severe case of COVID-19 showed higher concentrations of GFAP and NfL.

Glial Fibrillary Acidic Protien, or GFAP for short, is a known biomarker in the central nervous system (CNS) that is typically studied in those with brain injuries. When a brain injury occurs (concussion, retinal stess, tumors, etc.), GFAP is released into the blood stream and helps determine the severity of the injury. The results of this study help support and determine the relationship between COVID-19 and potentially lasting neural injuries.

To read this article in full, click here.

To learn more about how to measure GFAP, click here or contact us with your questions

The Eagle Biosciences MedFrontier FGF23 (Human Intact FGF23) CLEIA ELISA Assay was used in a recently published study looking at the association between FGF23 levels and major adverse cardiovascular events (MACE) and mortality in patients with type 2 diabetes and normal or mildly impaired kidney function.

FGF23 is an endocrine hormone involved in vitamin D metabolism and phosphorous level regulation. Previous studies have shown a link between insulin resistance and an increase in FGF23, which researchers believe affects renal phosphorous handling and leads to a higher risk of MACE.

The study did find evidence of a connection with FGF23 levels and an increased risk of MACE or mortality in participating patients.

Read more about this study here.

Contact us for more information about this kit.

Study Citation:
Fibroblast Growth Factor 23 and Mortality in Patients With Type 2 Diabetes and Normal or Mildly Impaired Kidney Function
Stanley M.H. Yeung, S. Heleen Binnenmars, Christina M. Gant, Gerjan Navis, Ron T. Gansevoort, Stephan J.L. Bakker, Martin H. de Borst, Gozewijn D. Laverman
Diabetes Care Sep 2019, dc190528; DOI: 10.2337/dc19-0528

Eagle Biosciences partner Fianostics completed a study evaluating their Noggin and Asporin FluoBolt assays as biomarkers for non-alcoholic fatty liver disease (NAFLD). The study shows that NOGGIN and ASPORIN may be valuable biomarkers for the diagnosis of NAFLD patients and they may also mediate the favorable effect of vitamin E treatment, although mechanistic studies are needed. Further studies with higher patient numbers are also required to confirm these promising results. The study helps support that these highly sensitivity assays allow researchers to measure a decrease of both markers in samples from NAFLD patients. This measurement is not possible with less sensitive methods. This indicates that noggin and asporin may be valuable biomarkers for NAFLD diagnosis.

Read More

FluoBolt Kits:
Noggin
Asporin

Contact us for more information about these kits or our other FluoBolt offering.

The Eagle Biosciences NT-proCNP ELISA Assay Kit (manufactured by Biomedica) was used in a recent study published out of the University of Otago in Christchurch, New Zealand. This kit is used for the quantitative determination of NT-proCNP in human serum and plasma (EDTA, citrate, heparin). CNP, C-type natriuretic peptide, along with other natriuretic peptides, plays a role in regulatory mechanisms including blood pressure and body fluid homeostasis. It also serves as a biomarker.

Plasma C-Type Natriuretic Peptide: Emerging Applications in Disorders of Skeletal Growth

Abstract


Although studies in experimental animals show that blood levels of C-type natriuretic peptide (CNP) and its bioinactive aminoterminal propeptide (NTproCNP) are potential biomarkers of long bone growth, a lack of suitable assays and appropriate reference ranges has limited the application of CNP measurements in clinical practice. Plasma concentrations of the processed product of proCNP, NTproCNP – and to a lesser extent CNP itself – correlate with concurrent height velocity throughout all phases of normal skeletal growth, as well as during interventions known to affect skeletal growth in children. Since a change in levels precedes a measurable change in height velocity during interventions, measuring NTproCNP may have predictive value in clinical practice. Findings from a variety of genetic disorders affecting CNP signaling suggest that plasma concentrations of both peptides may be helpful in diagnosis, provided factors such as concurrent height velocity, feedback regulation of CNP, and differential changes in peptide clearance are considered when interpreting values. An improved understanding of factors affecting plasma levels, and the availability of commercial kits enabling accurate measurement using small volumes of plasma, can be expected to facilitate potential applications in growth disorders including genetic causes affecting the CNP signaling pathway.

Espiner, E.; Prickett, T.; Olney, Robert; (2019). Plasma C-Type Natriuretic Peptide: Emerging Applications in Disorders of Skeletal Growth. Horm. Res. Paediatr., 90:345–357. DOI: 10.1159/000496544

Contact us for more information about this kit or our other natriuretic peptide assay kits.

The Eagle Biosciences Noradrenaline (Norepinephrine) Sensitive ELISA was used in a recent study. This highly sensitive assay kit is part of our veterinary and neurobiology product lines. It is intended for the detection of noradrenaline (norepinephrine) in biological samples including serum, plasma, tissue, and cell culture samples of mice and rats.

Renal Denervation and CD161a Immune Ablation Prevent Cholinergic Hypertension and Renal Sodium Retention

Abstract


Cholinergic receptor activation leads to premature development of hypertension and infiltration of pro-inflammatory CD161a+/CD68+ M1 macrophages into the renal medulla. Renal inflammation is implicated in renal sodium retention and the development of hypertension. Renal denervation is known to decrease renal inflammation. To determine the role of CD161a+/CD68+ macrophages and renal sympathetic nerves in cholinergic-hypertension & renal sodium retention. Bilateral renal denervation (RND) and immune ablation of CD161a+ immune cells was performed in young prehypertensive SHR followed by infusion of either saline or nicotine (15mg/kg/day) for two weeks. Immune ablation was conducted by injection of unconjugated azide-free antibody targeting rat CD161a. Blood pressure was monitored by tail cuff plethysmography. Tissues were harvested at the end of infusion. Nicotine induced premature hypertension, renal expression of the sodium-potassium-chloride co-transporter (NKCC2), increases in renal sodium retention, and infiltration of CD161a+/CD68+ macrophages into the renal medulla of animals. All of these effects were abrogated or prevented by RND and ablation of CD161a+ immune cells. Cholinergic activation of CD161a+ positive immune cells leads to the premature development of hypertension in SHR, at least partly, through increased renal expression of NKCC2 and renal sodium retention. Effects on chemotaxis of CD161a+ macrophages to the renal medulla, decreased renal expression of NKCC2, and renal sodium retention appear to play a part in the prevention of cholinergic hypertension as a result of RND. The CD161a+ immune cells are necessary and essential for this pro-hypertensive nicotine-mediated inflammatory response. Cholinergic receptor activation leads to premature development of hypertension and infiltration of pro-inflammatory CD161a+/CD68+ M1 macrophages into the renal medulla. Renal inflammation is implicated in renal sodium retention and the development of hypertension. Renal denervation is known to decrease renal inflammation. To determine the role of CD161a+/CD68+ macrophages and renal sympathetic nerves in cholinergic-hypertension and renal sodium retention. Bilateral renal denervation (RND) and immune ablation of CD161a+ immune cells was performed in young prehypertensive SHR followed by infusion of either saline or nicotine (15mg/kg/day) for two weeks. Immune ablation was conducted by injection of unconjugated azide-free antibody targeting rat CD161a. Blood pressure was monitored by tail cuff plethysmography. Tissues were harvested at the end of infusion. Nicotine induced premature hypertension, renal expression of the sodium-potassium-chloride co-transporter (NKCC2), increases in renal sodium retention, and infiltration of CD161a+/CD68+ macrophages into the renal medulla of animals. All of these effects were abrogated or prevented by RND and ablation of CD161a+ immune cells. Cholinergic activation of CD161a+ positive immune cells leads to the premature development of hypertension in SHR, at least partly, through increased renal expression of NKCC2 and renal sodium retention. Effects on chemotaxis of CD161a+ macrophages to the renal medulla, decreased renal expression of NKCC2, and renal sodium retention appear to play a part in the prevention of cholinergic hypertension as a result of RND. The CD161a+ immune cells are necessary and essential for this pro-hypertensive nicotine-mediated inflammatory response.

Raikwar, NS;Braverman, C;Snyder, PM;Fenton, RA;Meyerholz, DK;Abboud, FM;Harwani, SC; (2019). Renal Denervation and CD161a Immune Ablation Prevent Cholinergic Hypertension and Renal Sodium Retention. Am. J. Physiol. Heart Circ. Physiol.. doi:10.1152/ajpheart.00234.2019.

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