Human DEFB4 ELISA Kit (DEIA3322)

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

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cell lysates, plasma, serum
Species Reactivity
Intended Use
The Human DEFB4 ELISA Kit contains the components necessary for quantitative determination of natural or recombinant hBD-2 concentrations within any experimental sample including cell lysates, serum and plasma.
Contents of Kit
1. 96-Well Microplate or Strips Coated w/Capture Antibody. 12 x 8 Strips
2. Biotin-Conjugated Detection Antibody. Lyophilized Yellow 50 µL H2O Use Detection.
3. Ready to Use. Avidin-HRP Conjugate Solution. 11 mL
4. Cytokine Protein Standard. Lyophilized (100 ng). Red 100 µL H2O.
5. Ready-to-Use Substrate. 11 mL Brown
6. Stop Solution. 11 mL Clear
7. Adhesive Plate Sealers. 4 Sheets
8. Wash Buffer (10x). 50 mL Clear Dilute to 1X.
9. Protein Standard Diluent. 11 mL Clear
10. Detection Antibody Diluent. 11 mL Clear
Store components of the kit at 2-8°C or -20°C upon arrival up to the expiration date. For more detailed information, please download the following document on our website.
50 ng/mL


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Laser-activated transforming growth factor-1 induces human -defensin 2: implications for laser therapies for periodontitis and peri-implantitis


Authors: Tang, E.; Khan, I.; Andreana, S.; Arany, P. R.

BackgroundThere is increasing popularity of high-power lasers for surgical debridement and antimicrobial therapy in the management of peri-implantitis and periodontal therapy. Removal of the noxious foci would naturally promote tissue healing directly. However, there are also anecdotal reports of better healing around routine high-power laser procedures. The precise mechanisms mediating these effects remain to be fully elucidated. This work examines these low-dose laser bystander effects on oral human epithelial and fibroblasts, particularly focusing on the role of human -defensin 2 (HBD-2 or DEFB4A), a potent factor capable of antimicrobial effects and promoting wound healing. Material and MethodsLaser treatments were performed using a near-infrared laser (810 nm diode) at low doses. Normal human oral keratinocytes and fibroblast cells were used and HBD-2 mRNA and protein expression was assessed with real time polymerase chain reaction, western blotting and immunostaining. Role of transforming growth factor (TGF)-1 signaling in this process was dissected using pathway-specific small molecule inhibitors. ResultsWe observed laser treatments robustly induced HBD-2 expression in an oral fibroblast cell line compared to a keratinocyte cell line. Low-dose laser treatments results in activation of the TGF-1 pathway that mediated HBD-2 expression. The two arms of TGF-1 signaling, Smad and non-Smad are involved in laser-mediated HBD-2 expression. ConclusionsLaser-activated TGF-1 signaling and induced expression of HBD-2, both of which are individually capable of promoting healing in tissues adjacent to high-power surgical laser applications. Moreover, the use of low-dose laser therapy itself can provide additional therapeutic benefits for effective clinical management of periodontal or peri-implant disease.

Petrolatum: Barrier repair and antimicrobial responses underlying this "inert" moisturizer


Authors: Czarnowicki, Tali; Malajian, Dana; Khattri, Saakshi; da Rosa, Joel Correa; Dutt, Riana; Finney, Robert; Dhingra, Nikhil; Peng Xiangyu; Xu, Hui; Estrada, Yeriel D.; Zheng, Xiuzhong; Gilleaudeau, Patricia; Sullivan-Whalen, Mary; Suarez-Farinas, Mayte; Shemer, Avner; Krueger, James G.; Guttman-Yassky, Emma

Background: Petrolatum is a common moisturizer often used in the prevention of skin infections after ambulatory surgeries and as a maintenance therapy of atopic dermatitis (AD). However, the molecular responses induced by petrolatum in the skin have never been assessed. Objective: We sought to define the cutaneous molecular and structural effects induced by petrolatum. Methods: Thirty-six healthy subjects and 13 patients with moderate AD (mean SCORAD score, 39) were studied by using RT-PCR, gene arrays, immunohistochemistry, and immunofluorescence performed on control skin, petrolatum-occluded skin, and skin occluded with a Finn chamber only. Results: Significant upregulations of antimicrobial peptides (S100A8/fold change [FCH], 13.04; S100A9/FCH, 11.28; CCL20/FCH, 8.36; PI3 [elafin]/FCH, 15.40; lipocalin 2/FCH, 6.94, human beta-defensin 2 [DEFB4A]/FCH, 4.96; P < .001 for all) and innate immune genes (IL6, IL8, and IL1B; P < .01) were observed in petrolatum-occluded skin compared with expression in both control and occluded-only skin. Application of petrolatum also induced expression of key barrier differentiation markers (filaggrin and loricrin), increased stratum corneum thickness, and significantly reduced T-cell infiltrates in the setting of "normal-appearing" or nonlesional AD skin, which is known to harbor barrier and immune defects. Conclusions: Petrolatum robustly modulates antimicrobials and epidermal differentiation barrier measures. These data shed light on the beneficial molecular responses of petrolatum in barrier-defective states, such as AD and postoperative wound care.

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