The present study demonstrates that the anti-inflammatory activity of ASU and EGCG is potentiated when used in combination. This combination may offer an attractive supplement or alternative to non-steroidal anti-inflammatory drugs (NSAIDs) in the management of osteoarthritis.

These data show that HRV-16 infection or exposure to dsRNA induces epithelial B7-H1 and B7-DC.

Chondrocytes proliferated without loss of the cartilage phenotype. Responses to cytokines were significantly inhibited by the mixtures of ASU + GLU + CS and PPS + NG, which indicated that this response can be modulated. This culture technique can be used to study the functional properties of camel chondrocytes and identify agents that may potentially be used to treat and manage joint inflammation.

Osteoarthritis is characterized by inflammation and increased production of pro-inflammatory mediators including cytokines and prostaglandin E2 (PGE2). Macrophage-like cells in synovial tissue produce these mediators which induce degradative enzymes that break down cartilage. We determined whether avocado/soybean unsaponifiables (ASU) and chondroitin sulfate (CS) can inhibit cytokine expression and PGE2 production using monocyte/macrophage-like cell models. Cells were incubated for 24 hours with either control media alone, ASU alone (NMX1000; 8.3 μg/ ml), CS alone (TRH122; 20 μg/ml), or a combination of both preparations. Cells were activated with cytokines or lipopolysaccharide for 1 or 24 hours to determine cytokine gene expression by RT-PCR and PGE2 production by immunoassay, respectively. In response to activation, THP-1 cells exhibited increased expression of TNF-α and IL-1β, while RAW cells increased synthesis of PGE2. Cytokine expression and PGE2 synthesis were significantly decreased by the combination of ASU and CS compared to the individual treatments alone (P<0.05). Our finding supports the potential of the ASU and CS combination to suppress the synthesis of pro-inflammatory mediators in the joint.

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We have found that human airway epithelial cells express costimulatory molecules B7-H1, B7-H2, B7-H3 and B7-DC mRNA and cell-surface protein. IFN? and TNF? selectively induce B7-H1 and B7-DC and glucocorticoid fluticasone (FP) inhibits this induction. We now report that human rhinovirus infection (HRV-16), a key trigger of exacerbations of chronic rhinosinusitis and asthma, results in selective induction of B7-H1 and B7-DC expression in airway epithelial cells both in vitro and in vivo. In vitro exposure of human primary bronchial epithelial cells (PBEC) to HRV-16 (TCID50 5 X 103.1) resulted in induction of cell surface expression of B7-H1 as measured by flow cytometry (from 42±9 to 56±8 MFI, p&lt;0.05) and B7-DC (from 5±1 to 9±2 MFI, p&lt;0.01) (n=6). Pretreatment with FP (10-7 M) inhibited the induction of B7-H1 by 64% (p&lt;0.05) and B7-DC by 95% (p&lt;0.01). Additionally, in vitro exposure of PBEC to TLR3 agonist dsRNA (25 ug/ml), a surrogate for HRV16 infection, mirrored the effect of HRV-16 infection. Nasal scrapings taken at the time of peak symptom scores 4 days after infection of 6 human subjects with HRV-16 showed selective increases in levels of mRNA for B7-H1 (8.5±2.5 fold, p&lt;0.03) and B7-DC (3.2±1.1 fold, p&lt;0.07). These data show that exposure to TLR3 agonist dsRNA or HRV-16 infection induces B7-H1 and B7-DC on epithelial cells and this may influence the development of adaptive immune responses in the airways.

Rheumatoid arthritis (RA) synoviocytes present an increased mitochondrial genome mutagenesis, leading to mitochondrial alterations that might be participating in the pathogenesis of the disease. This study was performed to examine whether mitochondrial dysfunction is involved in joint destruction and inflammation in RA in relation to the expression of matrix metalloproteinases-1 and-3 (MMP-1 and MMP-3) and vascular endothelial growth factor (VEGF) in normal human synoviocytes. Methods: Normal human synoviocytes were treated with the commonly used mitochondrial respiratory inhibitor oligomycin (OLI) (10 mg/ml) for 24