15,16-Dihydrotanshindiol C

A 15-amino acid C-terminal peptide of beta-defensin-3 inhibits bone resorption by inhibiting the osteoclast differentiation and disrupting podosome belt formation.[Pubmed:28889177]

J Mol Med (Berl). 2017 Dec;95(12):1315-1325.

Human beta-defensin-3 (HBD3), which is secreted from cells in the skin, salivary gland, and bone marrow, exhibits antimicrobial and immunomodulatory activities. Its C-terminal end contains a 15-amino acid polypeptide (HBD3-C15) that is known to effectively elicit antimicrobial activity. Recently, certain antimicrobial peptides are known to inhibit osteoclast differentiation and, thus, we investigated whether HBD3-C15 hinders osteoclast differentiation and bone destruction to assess its potential use as an anti-bone resorption agent. HBD3-C15 inhibited the receptor activator of nuclear factor kappaB ligand (RANKL)-induced osteoclast differentiation and formation of resorption pits. In addition, HBD3-C15 disrupted the formation of RANKL-induced podosome belt which is a feature typically found in mature osteoclasts with bone-resorbing capacity. HBD3-C15 downregulated cortactin, cofilin, and vinculin, which are involved in the podosome belt formation. Furthermore, bone loss induced by RANKL was significantly reduced in a mouse calvarial implantation model that was treated with HBD3-C15. Similar inhibitory effects were observed on the osteoclast differentiation and podosome belt formation induced by Aggregatibacter actinomycetemcomitans lipopolysaccharide (AaLPS). Concordantly, HBD3-C15 attenuated the resorption in the calvarial bone of AaLPS-implanted mouse. Collectively, these results suggest that HBD3-C15 has an anti-bone resorption effect in developing osteoclasts and that this occurs via its disruption of podosome belt formation. HBD3-C15 could be a potential therapeutic agent for the inhibition of bone destruction. KEY MESSAGES: HBD3-C15 inhibits osteoclast differentiation and bone resorption capacity. HBD3-C15 disrupts the podosome belt formation in osteoclasts. HBD3-C15 alleviates the bone loss by RANKL or A. actinomycetemcomitans LPS in vivo.

Genomic sequences of two novel HLA-C alleles, HLA-C*15:143 and HLA-C*07:109:02.[Pubmed:28858436]

HLA. 2017 Dec;90(6):374-376.

Two novel HLA-C alleles, C*07:109:02 and C*15:143, were characterized in two Spanish individuals.

[Molecular characterization of non-vaccine Streptococcus pneumoniae serotypes 11A, 15 B/C and 23A recovered from invasive isolates in Colombia].[Pubmed:28968016]

Biomedica. 2017 Sep 1;37(3):390-396.

INTRODUCTION: A total of 192 invasive Streptococcus pneumoniae isolates, from serotypes 11A, 15B/C and 23A (not included in the conjugated vaccines), were collected in Colombia between 1994 and 2014 as part of the activities of the Network surveillance system for the causative agents of pneumonia and meningitis (SIREVA II). OBJECTIVE: To determine the molecular characteristics of invasive S. pneumoniae isolates from serotypes 11A, 15B/C and 23A in Colombia from 1994 to 2014. MATERIALS AND METHODS: The molecular characterization of the isolates was carried out through Pulse-Field Gel Electrophoresis (PFGE) and Multilocus Sequence Typing (MLST). RESULTS: Serotype 11A showed one clonal group represented by ST62. Serotype 15B/C was composed of three groups associated with Netherlands15B-37 ST199 (28.75%), ST8495 (18.75%), and SLV (Single-Locus Variant) of ST193 (21.25%). Isolates from serotype 23A were gathered in three clonal groups, with 70.21% closely related to ST42, 17.02% to Colombia23F-ST338, and 6.38% to Netherlands15B-37 ST199. CONCLUSION: Clones Colombia23F-ST338 and Netherlands15B-ST199 covered more serotypes than those previously found by other authors, including serotype 23A. These analyses reveal the importance of capsular switching in the spreading of successful clones among non-vaccine serotypes causing invasive pneumococcal disease.