Human BD-2 High-Sensitivity ELISA KIT (DEIA7829)

Regulatory status: For research use only, not for use in diagnostic procedures.

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Size
96T
Sample
serum, plasma
Intended Use
The Human Beta Defensin 2 (hBD-2) ELISA Kit is a sandwich ELISA kit for the quantification of BD-2 in cultures of human cells and in appropriately qualified samples from serum, saliva, or other tissue fluids. For research use only (RUO); not for therapeutic or diagnostic use.
Contents of Kit
1. Human Beta Defensin 2 Standard: Three (3) vials, each containing BD-2 lyophilized in buffer with proteins and antimicrobial. Refrigerate lyophilized vials until used or kit lot expires.
2. Sample Diluent Concentrate (20x): 10ml
3. Wash Solution Concentrate (100x): 10ml
4. Anti-Human Beta Defensin 2 Detection Antibody Concentrate (100x): 0.15ml
5. Streptavidin-HRP Conjugate Concentrate (100x): 0.15ml
Ready For Use: Store as indicated on labels.
6. Anti-Human Beta Defensin 2 Coated Strip Plate: 8-well strips (12), Coated with purified anti-Human BD-2 antibodies. Return unused strips to the pouch with desiccant; reseal and store refrigerated.
7. TMB Substrate: 12 ml, Chromogenic substrate for HRP containing TMB and peroxide.
8. Stop Solution: 12 ml, 1% sulfuric acid.
Storage
The microtiter well plate and all other reagents, if unopened, are stable at 2-8°C until the expiration date printed on the label. Stabilities of the working solutions are indicated under Reagent Preparation.

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References


Gastric Antimicrobial Peptides Fail to Eradicate Helicobacter pylori Infection Due to Selective Induction and Resistance

PLOS ONE

Authors: Nuding, Sabine; Gersemann, Michael; Hosaka, Yoshio; Konietzny, Sabrina; Schaefer, Christian; Beisner, Julia; Schroeder, Bjoern O.; Ostaff, Maureen J.; Saigenji, Katunori; Ott, German; Schaller, Martin; Stange, Eduard F.; Wehkamp, Jan

Background: Although antimicrobial peptides protect mucus and mucosa from bacteria, Helicobacter pylori is able to colonize the gastric mucus. To clarify in which extend Helicobacter escapes the antimicrobial defense, we systematically assessed susceptibility and expression levels of different antimicrobial host factors in gastric mucosa with and without H. pylori infection. Materials and Methods: We investigated the expression levels of HBD1 (gene name DEFB1), HBD2 (DEFB4A), HBD3 (DEFB103A), HBD4 (DEFB104A), LL37 (CAMP) and elafin (PI3) by real time PCR in gastric biopsy samples in a total of 20 controls versus 12 patients colonized with H. pylori. Immunostaining was performed for HBD2 and HBD3. We assessed antimicrobial susceptibility by flow cytometry, growth on blood agar, radial diffusion assay and electron microscopy. Results: H. pylori infection was associated with increased gastric levels of the inducible defensin HBD2 and of the antiprotease elafin, whereas the expression levels of the constitutive defensin HBD1, inducible HBD3 and LL37 remained unchanged. HBD4 was not expressed in significant levels in gastric mucosa. H. pylori strains were resistant to the defensins HBD1 as well as to elafin, and strain specific minimally susceptible to HBD2, whereas HBD3 and LL37 killed all H. pylori strains effectively. We demonstrated the binding of HBD2 and LL37 on the surface of H. pylori cells. Comparing the antibacterial activity of extracts from H. pylori negative and positive biopsies, we found only a minimal killing against H. pylori that was not increased by the induction of HBD2 in H. pylori positive samples. Conclusion: These data support the hypothesis that gastric H. pylori evades the host defense shield to allow colonization.

Tissue-engineered human psoriatic skin supplemented with cytokines as an in vitro model to study plaque psoriasis

REGENERATIVE MEDICINE

Authors: Pouliot-Berube, Claudia; Zaniolo, Karine; Guerin, Sylvain L.; Pouliot, Roxane

Aim: Psoriasis is a chronic inflammatory skin disease. To study its complex etiology, a psoriatic skin substitute model supplemented with a cytokine cocktail has been used. Materials & methods: Reconstructed psoriatic skin substitutes were supplemented with a cocktail of four cytokines: TNF-alpha, IL-1 alpha, IL-6 and IL-17A, to monitor their impact on gene expression by DNA microarray. Results: Gene profiling analyses identified several deregulated genes reported as being also deregulated in psoriasis skin in vivo (S100A12, IL-8, DEFB4A and KYNU). The expression of those genes was dramatically increased compared with basal levels of controls (p < 0.005 to < 0.05). Conclusion: Psoriatic substitutes supplemented with a cocktail of TNF-alpha, IL-1 alpha, IL-6 and IL-17A showed similar transcriptome alterations to those found in psoriasis.

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