Baseline characteristics.

<p>Data are given as median (min-max) except when percentage is indicated.</p><p>HbA1c: n = 18 (high HDL); FFA: n = 18 (high HDL); LDL: n = 14 (low HDL).</p><p>Low and High HDL groups.</p

Increased plasma levels of IL-9 in patients with carotid and coronary atherosclerosis.

<p>Panel <b>A</b> shows plasma levels of IL-9 in patients with asymptomatic (n = 56) and symptomatic (n = 88) carotid plaques and in healthy controls (n = 28). Panel <b>B</b> shows plasma levels of IL-9 in patients with STEMI (n = 42) at admission and at different time points after PCI (2, 7 and 60 days). For comparison, levels were also measured in healthy controls (n = 10). Data are presented as mean±SEM. *p<0.05, **p<0.01 and ***p<0.0001 versus controls. #p<0.05 and ##p<0.01 versus levels at admission.</p

Levels of serum PON1 activity oxLDL and PBMC gene expression of PON2.

<p>Serum PON1 activity (A), PBMC gene expression levels of PON2 (B), serum oxLDL levels (C) in subjects with low HDL cholesterol levels (n = 15) and subjects with high HDL cholesterol levels (n = 19; n = 18 for PON1 activity and oxLDL). The horizontal bars represent median values.</p

PBMC gene expression levels of cholesterol efflux mediators.

<p>ABCA1 (A), ABCG1 (B), SR-B1 (C), CD36 (D) and SR-A (E) in subjects with low HDL cholesterol levels (n = 15) and subjects with high HDL cholesterol levels (n = 19). The horizontal bars represent median values.</p

Multi-Block Partial Least Squares Regression (MBPLSR) analysis of the data after three weeks of intervention.

<p>First and second PLSR components of block scores of ceramides, lysoPC, lysoPE, PA, PC and PE are shown (A–F). The samples of each intervention group are presented as blue (HOSO group) or red (FO group) circles. The (un-validated) explained variances are shown on the axes.</p

Increased expression of IL-9 and IL-9R in immune cells from patients with coronary atherosclerosis.

<p>mRNA levels of IL-9 and IL-9R were quantified by real-time RT-PCR in CD3⁺ T cells (<b>A</b> and <b>B</b>) and in monocytes (<b>C</b>) from healthy controls (n = 11) and from patients with stable (SAP, n = 11) and unstable (UAP, n = 17) angina. mRNA levels are related to the reference gene 18S (T cells) and β-actin (monocytes) and normalized to levels in healthy controls. For monocyte analyses, only samples from 9 of the controls and 13 of the patients with unstable angina were available. No IL-9R transcripts were detected in patients or controls in these cells. Bars represent mean±SEM. #p<0.05 versus stable angina, *p<0.05 and **p<0.01 versus controls.</p

Cross-validated explained variance in Y.

<p>Bar plots of the validated explained variances in <b>Y</b> for each block and for the global model using data obtained after three weeks of intervention are presented.</p

Increased expression of IL-9 and IL-9R in human atherosclerotic carotid plaques.

<p>mRNA levels of IL-9 (<b>A</b>) and IL-9R (<b>B</b>) in patients with asymptomatic (n = 13) and symptomatic (n = 55) carotid stenosis and in non-atherosclerotic vessels obtained from organ donors (common iliac artery, n = 10) were quantified by real-time RT-PCR. No IL-9R transcripts were detected in control samples. Levels of IL-9 and IL-9R expression are related to reference gene β-actin. Data are presented as mean±SEM. ***p<0.0001 versus controls.</p

IL-9 promotes IL-17 release in PBMCs.

<p>PBMCs from healthy controls (Ctr, n = 5) and patients with unstable angina (UAP, n = 5) were stimulated with IL-9 (100 ng/ml) with and without co-stimulation with PHA (20 µg/ml). Panel <b>A</b> shows the absolute release of IL-17 after culturing for 72 hours as assessed by EIA measurements in cell-free supernatants (controls to the left, patients to the right). Panel <b>B</b> shows the percentage change in IL-17 release when adding IL-9 to unstimulated cells from healthy controls (left) and patients (right). Panel <b>C</b> shows the percentage change in IL-17 release when adding IL-9 to PHA-stimulated cells from healthy controls (left) and patients (right). Data are given as mean±SEM. *p<0.05 versus comparative condition without IL-9 (unstimulated and PHA stimulated, respectively). #p<0.05 versus healthy controls.</p

Flow chart of the study showing subjects enrolled, lost during follow-up and number of subjects included in the statistical analysis at baseline and after three and seven weeks of fish oil supplementation.

<p>FO group, fish oil group; HOSO, high oleic sunflower oil group; oxFO, oxidized fish oil group (not included in the present study).</p