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1.
Figure 5

Figure 5. The effect of EPA on TNF-induced surface adhesion molecule expression.. From: Omega-3 Fatty Acids and Inflammation: Novel Interactions Reveal a New Step in Neutrophil Recruitment.

The expression of (A) E-selectin and (B) VCAM-1 was measured by ELISA in TNF-stimulated endothelial cells that were either unsupplemented or supplemented with EPA. Data are mean±SEM of seven experiments. ANOVA showed that there was a significant effect of the dose of TNF (p<0.01), but not of EPA, on the expression of both receptors.

Samantha P. Tull, et al. PLoS Biol. 2009 August;7(8):e1000177.
2.
Figure 3

Figure 3. The effects of EPA supplementation on the fatty acid content of endothelial cell phospholoipds.. From: Omega-3 Fatty Acids and Inflammation: Novel Interactions Reveal a New Step in Neutrophil Recruitment.

(A and B) The concentration of EPA in membrane phospholipids was increased after supplementation of culture medium with EPA for 24 h. Error bars indicate SEM. AA, arachidonic acid; FA, fatty acid; PA, palmitic acid; SA, stearic acid.

Samantha P. Tull, et al. PLoS Biol. 2009 August;7(8):e1000177.
3.
Figure 8

Figure 8. The effect of adhesion on the expression of l-selectin and CD11b on neutrophils.. From: Omega-3 Fatty Acids and Inflammation: Novel Interactions Reveal a New Step in Neutrophil Recruitment.

Neutrophils that were freshly isolated, migrated across endothelial cells stimulated with TNF or adherent to the surface of EPA-supplemented endothelial cells (EC) activated with TNF were harvested and the expression of (A) CD11b or (B) l-selectin (CD62L) assessed by flow cytometry. Data are mean±SEM of four experiments; ANOVA showed significant effect of treatments in (A) (p<0.01) and (B) (p<0.05). In (A and B), Dunnett's test showed significant difference between −EPA and freshly isolated cells (*p<0.01 and *p<0.05, respectively), but not between +EPA and freshly isolated cells.

Samantha P. Tull, et al. PLoS Biol. 2009 August;7(8):e1000177.
4.
Figure 6

Figure 6. A cyclooxygenase (COX)-derived eicosanoid is required for neutrophil transmigration across TNF-stimulated endothelial cells.. From: Omega-3 Fatty Acids and Inflammation: Novel Interactions Reveal a New Step in Neutrophil Recruitment.

(A) Inhibition of COX-1 (SC-560), COX-2 (NS-398), or both (indomethacin) caused inhibition of neutrophil transmigration, *p<0.05 by t-test. (B) Addition of AA to EPA-supplemented endothelial cells during the period of TNF stimulation restored neutrophil transmigration. All data are mean±SEM of four experiments. ANOVA showed significant effects of treatments in both (A and B) (p<0.01). In (A), Dunnett test showed significant effects of individual treatments compared to untreated control, *p<0.05. In (B), Dunnett's test showed significant difference between EPA-treated and untreated control (**p<0.01), but not between AA+EPA and control.

Samantha P. Tull, et al. PLoS Biol. 2009 August;7(8):e1000177.
5.
Figure 2

Figure 2. Chemokine signalling through CXCR2 is essential for neutrophil activation on TNF-stimulated endothelial cells.. From: Omega-3 Fatty Acids and Inflammation: Novel Interactions Reveal a New Step in Neutrophil Recruitment.

Using a flow-based adhesion assay, neutrophils isolated from whole blood were perfused across endothelial cells. Neutrophils were recruited to endothelial cells treated with TNF, but did not adhere to unstimulated endothelium. Detailed analysis of neutrophil behaviour showed that on TNF-stimulated endothelial cells, the majority of recruited cells transmigrated across the monolayer. When neutrophils were treated with anti-CXCR2, but not anti-CXCR1, neutrophil activation was inhibited so that nearly all of the recruited neutrophils rolled indefinitely on the monolayer and could not migrate; data are mean±SEM of four experiments **p<0.01 for comparison by paired t-test of neutrophil behaviour on TNF stimulated endothelial cells in the presence or absence of anti-CXCR2.

Samantha P. Tull, et al. PLoS Biol. 2009 August;7(8):e1000177.
6.
Figure 1

Figure 1. Steps in the process of neutrophil recruitment.. From: Omega-3 Fatty Acids and Inflammation: Novel Interactions Reveal a New Step in Neutrophil Recruitment.

Step 1: Neutrophils are captured from flow and tether and roll on tumour necrosis factor-α (TNF)-stimulated endothelial cells. Step 2: Neutrophils are then activated by the action of CXC-chemokines on the chemokine receptor, CXCR2, a process resulting in the activation of neutrophil β2-integrins. Step 3: β2-integrins engage counter receptors on the endothelial cell surface, and the neutrophil becomes stationary. Step 4: Prostaglandin-D2 (PGD2), generated by the action of cyclooxygenase enzymes on the n-6-PUFA arachidonic acid (AA), binds the PGD2 receptor, DP-1. DP-1 generates signals that stabilise neutrophil adhesion, induce neutrophil shape change, and support the process of transmigration across the endothelial cell monolayer. Step 5: If the endothelial cells have been supplemented with the n-3-PUFA, eicosapentaenoic acid (EPA), the alternative series prostanoid, PGD3, is generated, and this antagonises PGD2-mediated neutrophil responses.

Samantha P. Tull, et al. PLoS Biol. 2009 August;7(8):e1000177.
7.
Figure 7

Figure 7. The role of AA- and EPA-derived eicosanoids in neutrophil transmigration.. From: Omega-3 Fatty Acids and Inflammation: Novel Interactions Reveal a New Step in Neutrophil Recruitment.

(A) When PDG2 was perfused across a population of neutrophils adherent to EPA-treated endothelial cells, neutrophil transmigration was restored. However, PGD3 had no significant effect on neutrophil behaviour. All data are mean±SEM of four experiments. ANOVA showed significant effect of treatment on transmigration. *p<0.05 compared to EPA-supplemented endothelial cells in the absence of PGD2 by Dunnett test. (B) The DP1 receptor antagonist BW868c dose-dependently inhibited neutrophil transmigration on TNF-stimulated endothelial cells. All data are mean±SEM of five experiments; ANOVA showed a significant effect of BW868c concentration (p<0.01). (C) Perfusion of the DP-1 receptor agonist, BW245C, across neutrophils adherent to EPA-supplemented endothelial cells restored neutrophil migration to control levels. Data are mean±SEM of five experiments. ANOVA showed a significant effect of treatment on transmigration. **p<0.01 compared to EPA-supplemented endothelial cells in the absence of BW868C by Dunnett test. (D) Neutrophils perfused across TNF-stimulated endothelial cells in the presence of PGD3 showed a significantly reduced ability to migrate across the monolayer. Data are mean±SEM of three experiments; ANOVA showed a significant effect of PGD3 concentration on transmigration (p<0.01). (E) The levels of PGD3 released from endothelial cells are increased after EPA supplementation. Data are mean±SEM of three experiments. ANOVA showed a significant effect of treatment (p<0.05). **p<0.01 for PGD3 production compared to endothelial cells activated with TNF without EPA supplementation by Dunnett's test.

Samantha P. Tull, et al. PLoS Biol. 2009 August;7(8):e1000177.
8.
Figure 4

Figure 4. The effects of EPA supplementation on the adhesive behaviour of neutrophils.. From: Omega-3 Fatty Acids and Inflammation: Novel Interactions Reveal a New Step in Neutrophil Recruitment.

(A) EPA supplementation did not affect the number of neutrophils initially adhering to endothelial cells from flow. (B) However, the time course of neutrophil behaviour on TNF-stimulated endothelial cells showed that EPA supplementation drastically altered neutrophil behaviour. Thus, the number of activated and surface adherent neutrophils decreased with time in the presence or absence of EPA. However, on endothelium that had not been supplemented with EPA, this was because neutrophils transmigrated across the monolayer, whereas on EPA-supplemented endothelium this was because activated cells reverted back to a rolling form of adhesion. ANOVA showed that there was a significant effect of treatment (i.e., ±EPA) on the percentage of cells that were rolling, surface adherent, or transmigrated (p<0.01). In addition, there was a significant effect of time on each form of behaviour for the EPA-treated cells (p<0.05−0.01). Bonferroni tests showed significant differences at specific time points as marked; **p<0.01. (C) Inhibition of neutrophil transmigration was evident at levels of EPA supplementation as low as 50 nM. Data are mean±SEM of five experiments. ANOVA showed significant effects of treatment (p<0.05); *p<0.05 compared to untreated control by Dunnett's test. Error bars indicate SEM.

Samantha P. Tull, et al. PLoS Biol. 2009 August;7(8):e1000177.

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