Lipopolysaccharide levels at various stages of TB infection and during therapy.

<p>Lipopolysaccharide (LPS) concentrations (pg/ml) in plasma from A) patients with LTBI (n = 6) and active TB (n = 19) at baseline and after 8 and 24 weeks of anti-TB therapy and B) active TB (n = 10) at baseline and after 2 weeks of anti-TB therapy. Horizontal lines represent the median values. Significant p values (<.05) between groups and time-points are indicated.</p

Correlations between sCD14 and inflammation markers.

<p>Correlations between inflammation markers in the active TB group (n = 19) between A) CRP and sCD14 (r = 0.492, p = 0.032), B) ESR and sCD14 (r = 0.438, p = 0.060).</p

Demographic and clinical characteristics of study participants.

1<p>Interquartile range in brackets.</p>2<p>Including two native Norwegians.</p>3<p>All native Norwegians.</p>4<p>≥2 of the following symptoms: fever (temperature>38°C), weight loss, wasting, cough and night-sweat.</p

sCD14 levels at various stages of TB infection and during therapy.

<p>Soluble CD14 concentrations (ng/ml) in plasma from A) patients with LTBI (n = 6) and active TB (n = 19) at baseline and after 8 and 24 weeks of anti-TB therapy and B) active TB (n = 10) at baseline and after 2 weeks of anti-TB therapy. Horizontal lines represent the median values. Significant p values (<.05) between groups and time-points are indicated.</p

Lipoarabinomannan (LAM) detected by the Lipopolysaccaride (LPS) assay.

<p>Relation between Lipoarabinomannan (LAM) standard concentrations from the Enzyme-linked immunosorbent assay (ELISA) kit and Lipopolysaccaride (LPS) concentrations analysed by the Limulus Amebocyte Lysate colorimetric assay (LAL).</p

Myeloid differentiation-2 levels at various stages of TB infection and during therapy.

<p>Myeloid differentiation-2 (MD-2) concentrations (ng/ml) in plasma from patients with LTBI (n = 6) and active TB (n = 19) at baseline and after 2, 8 and 24 weeks of anti-TB therapy. Horizontal lines represent the median values. Significant p values (<.05) between groups and time-points are indicated.</p

Expression of CCL20 and Its Corresponding Receptor CCR6 Is Enhanced in Active Inflammatory Bowel Disease, and TLR3 Mediates CCL20 Expression in Colonic Epithelial Cells

<div><p>Background</p><p>The chemokine CCL20 and its receptor CCR6 are putative drug targets in inflammatory bowel disease, and CCL20 is a novel IBD predilection gene. Previous findings on the CCL20 response in these diseases are divergent. This study was undertaken to examine CCL20 and CCR6 during active and inactive disease, and mechanisms for CCL20 regulation by the innate immune system. As TLR3 has recently emerged as a possible mediator of CCL20 production, we hypothesised that this TLR plays an important role in enterocytic CCL20 production.</p><p>Methods</p><p>A large microarray study on colonic pinch biopsies from active and inactive ulcerative colitis and Crohn’s disease provided background information. CCL20 and CCR6 were localized and their expression levels assessed in biopsies using <i>in situ</i> hybridization and immunohistochemistry. Regulation of CCL20 was studied in the HT29 cell line using a panel of pattern recognition receptor ligands followed by a TLR3 siRNA assay.</p><p>Results</p><p><i>CCL20</i> and <i>CCR6</i> mRNA abundances were increased during active inflammation (<i>CCL20</i> 5.4-fold in ulcerative colitis and 4.2-fold in Crohn’s disease; <i>CCR6</i> 1.8 and 2.0, respectively). <i>CCL20</i> and <i>CCR6</i> mRNA positive immune cells in lamina propria were more numerous, and CCL20 immunoreactivity increased massively in the epithelial cells during active inflammation for both diseases. TLR3 stimulation potently induced upregulation and release of CCL20 from HT29 cells, and <i>TLR3</i> silencing reduced CCL20 mRNA and protein levels.</p><p>Conclusions</p><p>The CCL20-CCR6 axis is involved during active inflammation in both ulcerative colitis and Crohn’s disease. The epithelial cells seem particularly involved in the CCL20 response, and results from this study strongly suggest that the innate immune system is important for activation of the epithelium, especially through TLR3.</p></div

Counting of CCR6 positive cells in Immunohistochemistry and <i>in situ</i> hybridization.

<p>Number of positive staining cells given in mean ± SD. N = controls, UC = Ulcerative Colitis, CD = Crohn's Disease, a = active, i = inactive.</p><p>* p<0.05 versus control.</p><p>** p<0.01 versus control.</p><p>^# p<0.05 versus inactive disease.</p><p>^## p<0.01 versus inactive disease.</p><p>Counting of CCR6 positive cells in Immunohistochemistry and <i>in situ</i> hybridization.</p

Dataset for: Bronchial microdialysis monitoring of inflammatory response in open abdominal aortic aneurysm repair, an observational study

Hypothesis: Aortic surgery results in ischemia-reperfusion injury that induces an inflammatory response and frequent complications. The magnitude of the inflammatory response in blood and bronchi may be associated with the risk of immediate complications. Objectives: To evaluate bronchial microdialysis as a continuous monitoring of cytokines in bronchial epithelial lining fluid (ELF) and to determine whether bronchial ELF cytokine levels reflect the ischemia-reperfusion injury and risk for complications during open abdominal aortic aneurysm (AAA) repair. We measured cytokines in venous blood using microdialysis and in serum for comparison. Methods: Sixteen patients scheduled for elective open AAA repair were included in a prospective observational study. Microdialysis catheters were introduced into a bronchi and a cubital vein. Eighteen cytokines were measured using a Bio-Plex Magnetic Human Cytokine Panel. Measurements and Main Results: Samples were collected before and during cross-clamping of the aorta as well as from 0-60 min and from 60-120 min of reperfusion. The ELF levels of IL-5, IL-6, IL-13, GM-CSF, IL-2, IL-4 and TNF-α increased, whereas IL-7 decreased during reperfusion. Venous levels of IL-1β, IL-4, IL-6, IL-8, IL-10, IL-12, IL-17, MCP-1, MIP-1α, MIP-1β and TNF-α increased and exhibited their highest concentration during reperfusion. Both bronchial and venous cytokine levels correlated with duration of the procedure, critical care days and preoperative kidney disease. Three patients suffered organ failure as a direct consequence of the procedure, and in these patients the bronchial ELF concentrations of seventeen out of 18 cytokines differed significantly from patients without such complications. Conclusions: Bronchial microdialysis is suited for continuous monitoring of inflammation during open AAA repair. The bronchial ELF cytokine levels may be useful in predictin

CCL20 gene expression and protein release in TLR3 transfection assay.

<p><b>A:</b><i>TLR3</i> and <i>CCL20</i> mRNA abundance in poly (I:C) stimulated HT29 cells with and without TLR3 small interfering RNA(siRNA) transfection. Non-signalling siRNA is designated nsRNA, two different TLR3 specific siRNAs (TLR3.6 and TLR3.8) were used alone or in combination. The cells were transfected for 24 hours using TLR3 siRNAs or nsRNA and then stimulated with the TLR3 ligand poly (I:C) for 20 hours. Controls were unstimulated untranfected cells, poly (I:C) stimulated cells and cells treated with nsRNA stimulated with poly (I:C). ** p< 0.01 versus nsRNA, ## p<0.01 versus unstimulated control. Mean ± SD of triplicated is shown. <b>B:</b> The poly (I:C) effect on CCL20 release in HT29 cells after transfection with TLR3 siRNAs as described above. *** p< 0.001 versus nsRNA, #### p<0.0001 versus unstimulated control. Mean ± SD of triplicates is shown.</p