Beta-defensin 3 is a novel, non-hemolytic antimicrobial cationic peptide originally isolated from human lesional psoriatic scales and keratinocyte clones. It is a very small (2-6 kD) yet potent salt-insensitive broad spectrum antimicrobial that targets many pathogenic microbes such as multiresistant S. aureus, vancomyosin-resistant Enterococcus faecium, Gram-negative and Gram-positive bacteria, fungi, and enveloped viruses. The family of mammalian defensins are classified into alpha, beta and theta based on their size and pattern of disulfide bonding and all contain a six-cysteine motif that forms three intra-molecular disulfide bonds. Keratinocytes and airway epithelial cells are the primary cellular sources of beta-defensin-3. Tumor necrosis factor alpha (TNFalpha) and bacterial contact both induce beta-defensin-3 mRNA expression. It appears to be important in the innate epithelial defense of infections by various microorganisms that are present in skin and lung. More recent research implies that beta-defensin plays a key role beyond just antimicrobial – its functions could extend to chemoattraction, innate immune-mediated responses, and angiogenesis.
Immunohistochemistry-Paraffin: Defensin beta 3 Antibody
The beta-defensin 3 antibody enabled signal pathway mapping with regards to immune homeostasis as detailed by Weinberg's group at Case Western (1). Additionally, Western blotting with the beta-defensin 3 antibody by Zhu et al at factored in their primary study on the efficacy of beta-defensin 14 in treating osteomyelitis (2). Degeneration experiments by neurologists used the beta-defensin 3 antibody to correlate beta-defensin 3 with muscle fiber degeneration in idiopathic muscle inflammatory conditions (3). Very recent immunolocalization studies from Stoeckelhuber's group used the beta-defensin 3 antibody to characterize antimicrobial and cytoskeletal components within the human sinonasalmucosa (4). Studies from Kozar et al used the beta-defensin 3 antibody to monitor minute alterations in both quantity and distribution of natural antimicrobials in the rat small intestine ileum and jejunum resulting from ischemia-reperfusion injuries (5). They pursued this avenue of investigation because they postulated that the compounds would be upregulated in specifically defined areas stimulated to initiate protective mechanisms and respond with subsequent permeability changes and cellular disruption.
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