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Two new Calprotectin ELISA's have been released for quantitative determination of Calprotectin: HK382 & HK379.

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Posted in Product News By K. Peeters

New! Mouse Complement Pathway Assays!

May 13, 2016 2:42:34 AM

The activation of the lectin complement pathways in mice can now be measured with the new Hycult Biotech Assays HIT420 and HIT421.

Mouse Classical Complement Pathway Assay (HIT420)

Mouse Lectin Complemement Pathway Assay (HIT421)

The innate immune system is important in the first defense against foreign pathogens. A major component of this response is the complement system. Complement activation proceeds in a sequential fashion through the proteolytic cleavage of a series of proteins leading to the generation of activated products that mediate various biological activities through their interaction with specific cellular receptors and other serum proteins. The three pathways, designated classical, lectin and alternative pathway, converge at a central component into a final common pathway. That is activation of C3 leading to formation of C3a and C3b. This cleavage activates the terminal complement pathway leading to eventually the formation of the terminal C5b-9 complement complex (TCC).

The complement pathway assays are a new alternative for the AP50 and CH50 tests, that are more cumbersome and variable due to the fact that the test is performed with sheep erythrocytes. The mouse pathway Assays are easy to use and specific for its pathway by making use of a combination of specialized coatings and buffers. Complement deficiencies or other defects in the complement system can easily be screened by running this assay.

Posted in Product News By K. Peeters

Findings indicate that α-defensins and bacterial/permeability-increasing protein are related to obesity parameters.

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Posted in Scientific Publications By K. Peeters

Short summary of Bastaki, S et al; Effect of turmeric on colon histology, body weight, ulcer, IL-23, MPO and glutathione in acetic-acid-induced inflammatory bowel disease in rats

Inflammatory bowel disease (IBD) is characterized by recurrent ulceration of the bowel and is of unknown etiology. The pathogenesis likely involves genetic, environmental, and immunologic factors.

The use of medicinal plants or their active components is becoming an increasingly attractive approach for the treatment of various inflammatory disorders among patients unresponsive to steroids or unwilling to take standard medications. Food derivatives are increasingly being used as therapy for IBD because of limited toxicity. During the last ten years, a large number of dietary components have been evaluated as potential chemopreventive agents.

Turmeric, the powdered rhizome of the medicinal plant, Curcuma longa (CL) Linn, of the Zingiberaceae family is widely used as a food flavouring and colouring agent in the Asian cuisine. Curcumin has been used since ancient times for its medicinal property in India and Southeast Asia and is known to possess a variety of pharmacological effects including anti-inflammatory activities.

 

The effect of CL on mean colon myeloperoxidase levels in rats administered orally for 3 days before or 30 min after the induction of IBD was measured to determine the extent of inflammation. IBD significantly increased MCMPO levels in the untreated group (IBD, no CL) after 2 days of IBD. However, CL significantly reduced MCMPO levels at 2, 4 and 7 days of IBD, respectively. When CL was post-administered 30 min after the induction of IBD, CL significantly reduced the MCMPO levels in the untreated group (IBD, no CL) at 2, 4 and 7 days of IBD, respectively.


Posted in Scientific Publications By K. Peeters

C5a: a promising therapeutic target

Mar 25, 2016 4:29:00 AM

Short summary related to C5a from Wezel, A; Innate immune modulation in atherosclerosis and vascular remodeling, dissertation University Leiden 2014

High numbers of activated mast cells are detected in the rupture-prone shoulder regions of human atherosclerotic plaques. An increased amount of mast cells in the plaque of patients suffering from carotid artery stenosis is even found to correlate with intraplaque hemorrhage and the occurrence of future cardiovascular events. Moreover, a causal role is established linking mast cell activation to both atherosclerotic plaque growth and destabilization.

Mast cell activation in the context of atherosclerosis may be induced by various ligands. For instance, the bioactive lysophospholipid acid (LPA) is present in atherosclerotic plaques, and local administration of LPA in apoE-/- mice results in increased mast cell activation and plaque destabilization. Other mast cell ligands present in the atherosclerotic plaque include C5a, substance P, neuropeptide Y, and  oxidized LDL, which may all contribute to mast cell activation, with subsequent aggravation of atherosclerosis.

Instead of complete mast cell stabilization, a different approach may also be used, for instance via the inhibition of a specific ligand responsible for one route of mast cell activation in the setting of atherosclerosis. One of these ligands which may be advantageous for drug targeting is complement factor C5a. Research has demonstrated adverse effects for C5a mediated mast cell activation on vein graft lesion development. Moreover, we have demonstrated that C5a itself has direct effects on late stage lesional disruptions, indeed making C5a a promising therapeutic target. Previous studies have reported increased serum levels of C5a in patients with CVD; also, high C5a serum levels directly before stent placement have been correlated with increased in-stent restenosis. The therapeutic potential in cardiovascular disease of a C5 inhibitor, the monoclonal antibody Pexelizumab, has already been tested in phase III trials. For instance, patients undergoing coronary artery bypass surgery and reperfusion therapy for myocardial infarction have received treatment with Pexelizumab. Interestingly, a systemic meta-analysis pointed out that Pexelizumab was associated with a 26% reduction in risk of death after coronary artery bypass surgery.

Taken together, these data indicate that C5a may be a promising therapeutic target in the treatment of cardiovascular disease.

Posted in Scientific Publications By K. Peeters

LBP values higher with Obesity

Mar 24, 2016 5:58:47 AM

Short summary of Rodrigues, M et al; Obesity changes the human gut mycobiome. Nature, Scientific Report 2015

Research showed that the gut mycobiome differs between obese patients. The fungal microbiota (mycobiome) in obese and non-obese subjects was characterized using Internal Transcribed Spacer (ITS)-based sequencing. The results demonstrate that obese patients could be discriminated by their specific fungal composition. LBP is one of the biomarkers related to obesity.


LBP and obesity

 

Relationships between human mycobiome and anthropometric and metabolic parameters. Heat map showing associations of phylum, class, family and genus with clinical and anthropometrical data. The heat map is organized with fungi in rows and metabolic parameters in columns.


Posted in Scientific Publications By K. Peeters

Serum ficolin-3: potential to be a good prognostic predictive biomarker after head trauma

Short summary of Pan, J et al; Low serum ficolin-3 levels are associated with severity and poor outcome in traumatic brain injury. Journal of Neuroinflammation (2015) 12:226

In recent years, the application of biomarkers identified in the peripheral blood has shown potential clinical utility in neurointensive care as diagnostic, prognostic, and monitoring adjuncts. Evidence from experimental, clinical, and in vitro studies highlights an important role for ficolinmediated activation of the lectin pathway of complement in contributing to inflammation within the injured brain.

Compared with the healthy controls, serum ficolin-3 levels on admission were statistically decreased in patients with severe traumatic brain injury. Ficolin-3 was also identified as an independent prognostic predictor for 1-week mortality,6-month mortality, and 6-month unfavorable outcome.

https://static-content.springer.com/image/art%3A10.1186%2Fs12974-015-0444-z/MediaObjects/12974_2015_444_Fig1_HTML.gif 

 

Graph showing change of serum ficolin-3 levels after severe traumatic brain injury

 

 




Posted in Scientific Publications By K. Peeters

C1q level, a surrogate or prediction marker?

Short summary of Cho KJ et al; Apoptosis signal-regulating kinase 1 mediates striatal degeneration via the regulation of C1q. Sci Rep 2016, 6: 18840

Apoptosis signal-regulating kinase-1 (ASK1), an early signaling element in the cell death pathway, has been hypothesized to participate in the pathology of neurodegenerative diseases. The systemic administration of 3-nitropropionic acid (3-NP) facilitates the development of selective striatal lesions.

Recently, it has been proposed that complement-mediated synapse elimination may be reactivated aberrantly in the pathology of neurodegenerative diseases.

ASK1 may be involved in regulation of astrocyte TGF-beta and it is linked to the C1q level in spatial and temporal, and moreover in the earlier stage of progressing striatal neuronal loss. Conclusively the present study suggests that ASK1 mediates 3-NP toxicity and regulates C1q level through the astrocyte TGF-beta. It may also suggest that C1q level may be a surrogate of prediction marker representing neurodegenerative disease progress before developing behavioral impairment.

The infusion of 3-NP leads to selective striatal neuronal loss as well as astrocyte reactivation. Results from 3-NP-infused mouse blood serum revealed that the secretion levels of C1q were increased on day four when the lesion was not yet detectable and on day seven when the lesion was detectable in 3-NP infused mice.

 

C1q promotes arterial remodeling

Short summary of Yabumoto C et al; Angiotensin II receptor blockade promotes repair of skeletal muscle through down-regulation of aging-promoting C1q expression. Sci Rep 2015, 5: 14453

Down-regulation of the aging-promoting C1q mediated beneficial effects of AT1 receptor blockade on muscle repair and regeneration. We recently identified C1q as a diffusible factor in the serum that activates canonical Wnt/β -catenin signaling by binding to Wnt receptor Frizzled and by inducing cleavage of Wnt coreceptor LRP618. Serum and tissue concentrations of C1q showed a significant increase with aging, and C1q-mediated activation of Wnt/β -catenin signaling led to aging-related decline in regeneration capacity of skeletal muscles. C1q treatment attenuated satellite cell proliferation and stimulated fibroblast proliferation both in vitro and in vivo. We also reported that M2 macrophages were recruited to the aorta and secreted C1q, which promoted arterial remodeling through activation of Wnt/β -catenin signaling, in Ang II-infused mice.

We propose that AT1 receptor blockade reduces systemic and local levels of C1q through inhibiting C1q production by infiltrated macrophages, and thereby enhances activation and proliferation of satellite cells. Insomuch as AT1 receptor is expressed in both myocytes and macrophages, further studies will be required to elucidate the cell type-specific role of AT1 receptor in inducing C1q expression in macrophages in injured muscles.

 

Serum C1q concentrations in mice treated with irbesartan or vehicle at 4 days after cryoinjury or sham operation (n = 12, in each group). Data are presented as mean ± SEM. *P < 0.05. NS, not significant.

Posted in Scientific Publications By K. Peeters

A recent paper was published in which the use of the Properdin ELISA kit was described in relation with sepsis. The results concluded that properdin levels were significantly decreased in patients with sepsis on admission.

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Posted in Scientific Publications By G. Snippe

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Posted in Hycult Biotech Scientific Publications By G. Snippe

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