Disease relevance of Defb3

• Recombinant mBD-3 peptide, produced from a baculovirus expression system, showed antimicrobial activity against P. aeruginosa PAO1 (MIC of 8 micrograms/ml) and Escherichia coli D31 (MIC of 16 micrograms/ml) in a salt-dependent manner [1].
• After instillation of Pseudomonas aeruginosa PAO1 into mouse airways, mBD-3-specific mRNA was upregulated significantly not only in large airways but also in the small bowel and liver [1].
• The kinetics of gene expression and the cellular source of murine beta -defensin-3 (mBD3) and murine beta -defensin-4 (mBD4) were determined in mouse models of progressive pulmonary tuberculosis and latent infection induced by high or low infecting doses, respectively [2].
• We conclude that mBD-3 is an inducible peptide with limited tissue expression during E. coli peritonitis [3].
• Synthetic mBD-3 inhibited the growth of E. coli, Pseudomonas aeruginosa, Staphylococcus aureus, and Candida albicans at concentrations from 25 to 50 microg/mL [3].

High impact information on Defb3

• In situ hybridization revealed mBD-11, mBD-12, and mEP2e expression in the columnar epithelium of the caput epididymis, contrasting with the predominant expression of mBD-3 in the capsule or septum of the whole epididymis [4].
• Analysis of a genomic clone of mBD-3 revealed two exons separated by a 1.7-kb intron [1].
• Under basal condition, mBD-3 transcripts were detected at low levels in epithelial cells of surface organs, such as the intestine and lung [1].
• The mBD-3 gene is localized at the proximal portion of chromosome 8, the site where genes for mouse alpha- and beta-defensins are found [1].
• In an E. coli peritonitis model, expression of mBD-3 mRNA was upregulated only in the esophagus and tongue [3].

Chemical compound and disease context of Defb3

• Three of the tested compounds, 5-(p-nitrobenzamido)-2-benzylbenzoxazole (BD-3), 6-methyl-2-(o-chlorophenyl) benzoxazole (A-9) and 5-(p-nitrophenoxyacetamido)-2-phenylbenzoxazole (D-30), showed an increased apoptotic effect on mouse lymphoma cells [5].

Biological context of Defb3

• The purpose of this study was to determine the antimicrobial activity of mBD-3, the tissue distribution of mBD-3 expression, and the effect of gram-negative bacterial infection on mBD-3 expression [3].
• Moreover, compounds BD-3, A-9 and 5-(2-thienylcarboxyamido)-2-phenylbenzoxazole (D-24) also amplified the apoptosis effect of 12H-benzo(a)phenothiazines (M-627) [5].

Other interactions of Defb3

• Gf C57BL/6 and BALB/c mice expressed significantly different basal levels of mBD3, mBD4, TNF-alpha and IL-12 in gastric tissues; however, gf C57BL/6 and BALB/c mice were equally susceptible to intestinal colonization with C. albicans and had similar fungal burdens in gastric tissues 4 weeks after oral challenge [6].

Analytical, diagnostic and therapeutic context of Defb3

• Constitutive expression of mBD-3 mRNA was not consistently found in any organ using RT-PCR [3].
• The antimicrobial activity of synthetic mBD-3 was evaluated in microdilution broth assays using bacterial and fungal organisms. mBD-3 mRNA expression was assayed by polymerase chain reaction (PCR) using cDNA derived from a panel of tissues [3].

References