Adiponectin in gingival tissues and cultured oral epithelial cells.

<p>(A) Representative gingival tissue section from one out of 6 patients exhibiting adiponectin distribution assessed by immunohistochemistry with DAB-staining (brown color). (B) Higher magnification of the rectangular area shown in (A). (C) Immunofluorescence staining of adiponectin in cultured oral epithelial cells from one out of 6 patients. (D) Higher magnification of the rectangular area shown in (C). (E) Gene expression of adiponectin and its receptors AdipoR1 and AdipoR2 from oral epithelial cells of 2 patients (P1 and P2), as demonstrated by gel electrophoresis. (F) Gene expression of adiponectin and its receptors AdipoR1 and AdipoR2 from oral epithelial cells from 6 patients, as demonstrated by real-time PCR.</p

Effects of adiponectin on pro- and anti-inflammatory mediators.

<p>Effects of adiponectin (1 µg/ml) on IL1β, IL6 and IL8 (A) as well as IL10 and HMOX1 (B) in oral epithelial cells at 4 h, 8 h, and 24 h. Mean ± SEM; n = 6; * p<0.05 difference between adiponectin-treated and control cells.</p

Interactions of lipopolysaccharide and adiponectin on involucrin and growth factors.

<p>Effects of lipopolysaccharide (LPS; 2 µg/ml) and/or adiponectin (Adipo; 1 µg/ml) on the mRNA expression of involucrin, TGFβ1, and KGF at 4 h, 8 h, and 24 h expressed as fold of control. Mean ± SEM; n = 6;</p>*<p>p<0.05 different from control,</p>†<p>different from LPS-treated cells,</p>#<p>different from adiponectin-treated cells.</p

Effect of lipopolysaccharide and/or adiponectin on NFκB signaling.

<p>Effect of lipopolysaccharide (LPS; 2 µg/ml) and/or adiponectin (Adipo; 1 µg/ml) on the nuclear translocation of NFκB at 2 h. NFκB visualized by immunofluorescence (A). Quantitative analysis of immunofluorescence samples; evaluation as % NFκB positive nuclei (B).</p

Interactions of lipopolysaccharide and adiponectin on pro- and anti-inflammatory mediators.

<p>Effects of lipopolysaccharide (LPS; 2 µg/ml) and/or adiponectin (Adipo; 1 µg/ml) on the mRNA expression of IL1β (A), IL6 (C), IL8 (D), and IL10 (F) at 4 h, 8 h, and 24 h and on the protein level of IL1β (B) and IL8 (E) in supernatants at 24 h and 72 h. Mean ± SEM; n = 6; * p<0.05 difference between groups.</p

Interactions of lipopolysaccharide and adiponectin on cell viability.

<p>Effects of lipopolysaccharide (LPS; 2 µg/ml) and/or adiponectin (Adipo; 1 µg/ml) on the cell viability, as assessed by trypan blue exclusion test, at 24 h, 48 h, and 72 h. Mean ± SEM; n = 6;</p>*<p>p<0.05 different from control,</p>†<p>different from LPS-treated cells,</p>#<p>different from adiponectin-treated cells.</p

Interactions of lipopolysaccharide and adiponectin on matrix metalloproteinases.

<p>Effects of lipopolysaccharide (LPS; 2 µg/ml) and/or adiponectin (Adipo; 1 µg/ml) on the mRNA expression of MMP1 (A) and MMP3 (C) at 4 h, 8 h, and 24 h and on the protein level of MMP1 (B) in supernatants at 24 h and 72 h. Mean ± SEM; n = 6; * p<0.05 difference between groups.</p

Prevention of CASP induced aortic cytokine and iNOS production following TLR9 antagonist treatment.

<p><b>A-E</b> 24 h of exposure to the synthetic TLR9 antagonist H154-thioate did not induce mRNA expression of the investigated cytokines, but prevented the CASP-dependent rise in mRNA expression of inflammatory mediators. There was no observable influence of H154-thioate on iNOS expression. <b>F</b> H154-thioate treatment prior to CASP completely prevented the CASP-induced arterial hypocontractility observed in WT animals (F) (*p<0.05; **p<0.01; ***p<0.001; n≥5 animals in each group; mean ± SEM).</p

CASP induced aortic cytokine and iNOS production.

<p><b>A</b> Pro-inflammatory TNF-α was significantly up-regulated in WT mice compared to sham animals. CASP-surgery in TLR2-D animals lead to even higher levels of TNF-α compared to all other groups. <b>B, C</b> IL-1β and IL-6 were significantly up-regulated in TLR2-D animals after CASP compared to the other strains. <b>D</b> CASP induced a non-significant up-regulation of the anti-inflammatory cytokine IL-10 in WT, TLR2-D and CD14-D mice. <b>E</b> CASP induced a significant up-regulation of iNOS in TLR2-D mice only. (*p<0.05; **p<0.01; ***p<0.001; n≥5 animals in each group; mean ± SEM).</p

CpG oligonucleotide activates Toll-like receptor 9 and causes lung inflammation in vivo-4

<p><b>Copyright information:</b></p><p>Taken from "CpG oligonucleotide activates Toll-like receptor 9 and causes lung inflammation in vivo"</p><p>http://respiratory-research.com/content/8/1/72</p><p>Respiratory Research 2007;8(1):72-72.</p><p>Published online 9 Oct 2007</p><p>PMCID:PMC2173891.</p><p></p>hnique. CpG-ODN led to a significant increase in plasma cytokine levels of TNF-α and IL-6 within 2 hrs (mean ± SEM; * < 0.05)