IRF3 polymorphisms induce different innate anti-Theiler's virus immune responses in RAW264.7 macrophages.

Persistent viral infections can lead to disease such as myocarditis. Theiler's murine encephalomyelitis virus (TMEV) infects macrophages of SJL/J (H-2s) mice establishing persistent infections leading to demyelinating disease. In contrast macrophages from B10.

Incidence of endodontic implantitis and implant endodontitis occurring with single-tooth implants: a retrospective study.

The purposes of this study were to determine success and survival rates for implants and teeth adjacent to implants and the incidence of endodontic implantitis (E-I) (endodontic involvement in adjacent teeth causing implant failure) and implant endodontitis (I-E) (implant placement causing endodontic failure). The data were from 233 single-tooth implants placed in 116 subjects by postgraduate periodontal students with recall radiographs taken >or=9 months after implant placement. Three groups were analyzed: group A, implants with no adjacent teeth (n = 90); group B, implants with nonendodontically treated adjacent teeth (n = 123); and group C, implants with endodontically treated adjacent teeth (n = 20).

Promoter analysis reveals critical roles for SMAD-3 and ATF-2 in expression of IL-23 p19 in macrophages.

IL-23 p19/p40, produced by macrophages and dendritic cells, is critical for development of Th17 in several autoimmune diseases. In this study, bone marrow-derived (BMM) and splenic macrophages (SPM) from SJL/J mice, susceptible to autoimmune demyelinating disease following Theiler's virus (TMEV) infection, expressed IL-23 in response to TMEV. We identified potential binding sites for IFN response factor (IRF)-3 (nt -734 to -731), Sma- and Mad-related protein (SMAD)-3 (nt -584 to -581), activating transcription factor (ATF)-2 (nt -571 to -568), IRF-7 (nt -533 to-525), and NF-kappaB (nt -215 to -209) in the murine p19 promoter.

Human osteogenic protein-1 induces osteogenic differentiation of adipose-derived stem cells harvested from mice.

Objective: Osteogenic protein-1 (OP-1) has been shown to stimulate undifferentiated cells to produce mineralized tissue. Adipose tissue is a rich source of undifferentiated cells for tissue engineering purposes. The purpose of this study was to investigate the effect of OP-1 on osteogenic differentiation of adipose-derived stem cells and the production of bony tissue in vitro.

TLR3 and TLR7 are involved in expression of IL-23 subunits while TLR3 but not TLR7 is involved in expression of IFN-beta by Theiler's virus-infected RAW264.7 cells.

Theiler's murine encephalomyelitis virus (TMEV) infects macrophages and causes demyelinating disease (DD) in certain mouse strains. IL-23 p19/p40 and IFN-beta, which are both expressed by macrophages in response to TMEV, could contribute to or prevent DD. Because TMEV may induce macrophages' cytokines through TLR3 and TLR7 (toll-like receptors), their role in TMEV-induced IL-23 and IFN-beta expression by the RAW264.

Expression of IL-27 p28 by Theiler's virus-infected macrophages depends on TLR3 and TLR7 activation of JNK-MAP-kinases.

Theiler's murine encephalomyelitis virus (TMEV) causes a demyelinating disease (DD) due to infection of macrophages, stimulation of macrophage Toll-like receptor (TLR)3 and TLR7 pathways, activation of Mitogen-activated protein kinases (MAPK)s, and production of macrophages cytokines. Because expression of IL-27, a macrophage cytokine composed of p28 and EBI3 subunits, has been implicated in DD, we examined IL-27 subunit mRNA expression during TMEV infection of RAW264.7 cells, a macrophage cell line.