Low mineralization activity by human osteoblast cells (HOBs) indicates abnormal bone remodeling that potentially leads to osteoporosis. Oxidation, the most prominent form of high-density lipoprotein (HDL) modification, is suggested to affect bone mineralization through the inflammatory pathway. Adiponectin, which possesses anti-inflammatory activity, is postulated to have the ability to suppress the detrimental effects of oxidized HDL (oxHDL). This study aimed to investigate the effects of HDL before and after oxidation on markers of mineralization and inflammation. The protective effects of adiponectin on demineralization and inflammation induced by oxHDL were also investigated. OxHDL at 100 µg/mL protein had the highest inhibitory effect on mineralization, followed by lower calcium incorporation. OxHDL also had significantly lower expression of a mineralization marker (COL1A2) and higher expression of inflammatory markers (IL-6, TNF-α, and RELA proto-oncogene, NF-κβ (p65)) compared to the unstimulated control group. These findings suggest that oxHDL reduces the mineralization activity of HOBs by increasing the expression of inflammatory markers. Interestingly, co-incubation of adiponectin and oxHDL in HOBs resulted in higher expression of mineralization markers (ALPL, COL1A2, BGLAP, and RUNX2) and significantly reduced all targeted inflammatory markers compared to the oxHDL groups. On the contrary, HDL increased the expression of mineralization markers (COL1A2 and STAT-3) and exhibited lower expression of inflammatory cytokines (IL-6 and TNF-α), proving the protective effect of HDL beyond the reverse cholesterol transport activity.

[This corrects the article DOI: 10.1371/journal.pone.0116867.].

Background Viruses can utilise a variety of mechanisms to escape recognition and elimination by the host immune system. Here, we aim to exploit the UniProt database to identify Epstein-Barr virus (EBV) proteins with a function in immune system evasion (so-called ‘immunoevasins’) and to explore their associated biological processes and protein-protein interactions. Methods The UniProt database was used as the primary source for data mining. Keywords related to biological processes, including ‘immune system inhibition’ and ‘evasion’, were used. Only Swiss-Prot-reviewed proteins were included, and the retrieved data were further analysed by extracting information on annotation scores, gene ontologies and interactors. Further protein-protein interactions analysis was performed using the IntAct database. Results Our search in the UniProt database yielded 11 EBV proteins from 5 known EBV strains associated with host-immune evasion. The majority of the EBV proteins identified were involved in the inhibition of the host innate immune response. Others were related to the inhibition of adaptive host immune responses and the interferon signalling pathway. Protein-protein interactions analysis revealed four host proteins that have direct interaction with the EBV proteins. Conclusion Database mining has contributed to the rapid identification of curated EBV immunoevasins and identified the involved biological processes and relevant protein interactions.