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The above results show that CHRG01, a small peptides derived from human beta defensin-3 (HBD-3) without any complex structure, is capable of killing bacteria by permeabilizing their outer membranes.
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The results of the present study demonstrated that the transfected with HBD3 gene human periodontal ligament cells and bone marrow stromal cells stably expressed HBD3. In addition, periodontal pathogens and cariescausing bacteria were susceptible to the antimicrobial activity of the cells.
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Our results suggested that hBD3 is involved in the carcinogenesis and development of cervical cancer, and may serve as a biomarker or therapeutic target of this disease.
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These results indicated that hBD3 could have therapeutic effect on systemic inflammation associated with periodontal infections via modulating macrophage activation and orientation.
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Ablation of E6 by siRNA induces the tumor suppressor p53 and diminishes beta-defensin-3 (hBD3) in HPV-16 positive CaSki cervical cancer cells and UM-SCC-104 head and neck cancer cells.
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our findings provide new insights into the molecular mechanisms how HBD2 and HBD3 interact with cells of myeloid origin and demonstrate their immuno-modulating functions during innate immune responses.
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our work has revealed that hBD3 exhibits potent anti-inflammatory properties both in vitro and in vivo, and this effect might be correlated with inhibition of MAPK pathway
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hBD3 exhibits potent anti-periodontitis properties both in vitro and in vivo, and this effect may be correlated to inhibition of the nuclear factor-kappaB pathway and macrophage polarization.
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Different dynamics and pathway of disulfide bonds reduction has been demonstrated for two human defensins, HD5 and HBD-3.
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In this study, the results showed genetically modified (GM) milk containing human beta-defensin-3 (HBD3) was easy to be digested in simulated gastric fluid, and it did not have adverse effects on general and gastrointestinal (GI) tract health compared to conventional milk.
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Direct interaction between SP-A or SAP01 and human BD-3 seemed to be responsible for the inhibitory effects on chemotaxis of mast cells.
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Expression of hBD-1, hBD-2, hBD-3, and hBD-4 in healthy and chronic periodontitis gingiva.
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Per duplication of mRNA in whole blood, the risk of being a carrier increased by 93% for IL17A and decreased by 35% for IFN-gamma. Independent of carriage and DEFB promotor haplotype, a 1-unit increase in IFN-gamma/IL-17A mRNA ratio led to a 24% increase in HBD3 mRNA in wounded skin. A low Th1 to Th17 mRNA ratio increases the risk of colonization, with HBD3 being a potential link.
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Analysis of TLR4 and HBD3 expression in epithelial cells demonstrates the key role of the innate immune factors in the pathogenesis of inflammatory and destructive periodontal lesions.
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study indicated that the expression of HBD-2 and HBD-3 mRNA and protein in lesions of cutaneous tuberculosis may be not consistent with that of tuberculids
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epidermal growth factor receptor (EGFR)activation via phosphorylation of EGFR via TAK1-p38alpha pathway, and subsequent internalization of EGFR are functionally linked to the induction of hBD3 in gastric epithelial cells infected with H. pylori.
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These results demonstrate that the gamma-core within HBD3 is the ancestral core of the full-length molecule and is a viable HDP per se, since it is endowed with the most important biological features of HBD3
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C-terminal 15-mer peptide within hBD3, designated as hBD3-3, has cell- and skin-penetrating activity, which can induce anti-inflammatory activity
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Study found that HBD2 bound tightly to Mc1r with an affinity similar to that of HBD3
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Using bone marrow derived macrophages from knockout mice we demonstrate that hBD3 suppresses the polyI:C-induced TLR3 response mediated by TICAM1 (TRIF), while exacerbating the cytoplasmic response through MDA5 (IFIH1) and MAVS (IPS1/CARDIF).
