Abstracts 4. Gemeinsamer Jahreskongress der ... - SWISS KNIFE
Abstracts 4. Gemeinsamer Jahreskongress der ... - SWISS KNIFE
Abstracts 4. Gemeinsamer Jahreskongress der ... - SWISS KNIFE
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swissknife spezial 06 12.06.2006 13:39 Uhr Seite 36<br />
red at the first dressing change, 2-3 days after trauma. VAC ® and Epigard ® -fluid was squeezed<br />
out of the foam and centrifuged at 2000g, 4°C for 20min, additionally patient’s serum<br />
was collected. Wound fluid, or patient’s serum was diluted with RPMI 1640 medium 1:10<br />
(v/v) and incubated with freshly isolated PMN from healthy volunteers (106/ml) for 16 hours.<br />
Apoptosis of PMN was detected by flowcytometry after staining with Annexin-V-FITC and propidium<br />
iodine. Data are given as mean ± SEM; significance level was set at p < 0.05 using<br />
two-tailed Student’s-t-test.<br />
Results: Incubation of PMN from healthy volunteers (n=12) with VAC ® -fluid significantly inhibited<br />
spontaneous apoptosis compared to Epigard ® -fluid (10.8 ± 1.2% vs. 26.6 ± 1.8%, p <<br />
0.05), where the apontaneous apoptosis was (47.3 ± 3.2%). Icubation of PMN with serum<br />
from VAC ® or Epigard ® treated patients led not to a significant change in PMN apoptosis rate.<br />
Conclusion: Increased formation of granulation in VAC ® -treated wounds contributes to better<br />
wound healing. Besides an induction of inflammation in the wound the continuous negative<br />
pressure generated by the VAC ® -system seems to induce a local inflammation with an accumulation<br />
of neutrophils improving the wound healing.<br />
17.07<br />
L. Sun1 , T. Reding1 , M. Bain1 , U. Ungethüm1 , F. Storni1 , P. Clavien2 , D. Bimmler3 , R. Graf1 1Dept. of Visceral and Transplant Surgery, University Hospital of Zurich, 8091 Zurich/CH,<br />
2Swiss Hpb Center, Dept. Visceral and Transplant Surgery, University Hospital of Zurich, 8091<br />
Zurich/CH, 3Chirugie, Praxis, 8001 Zürich/CH<br />
Prostaglandin E2 and TN synergistically promote the expression of monocyte chemotactic<br />
protein-1 in the pancreatic acinar cell AR42J: interaction between macrophages and pancreatic<br />
acinar cells in pancreatitis<br />
Objective: MCP-1 is a strong chemoattractant for monocytes, macrophages and lymphocytes,<br />
and plays an important role in the recruitment of monocytes/macrophages in inflammatory<br />
tissues. In a model of chronic pancreatitis (WBN/Kob rat) we recently demonstrated that<br />
the inhibition of COX-2 activity reduces and delays inflammation. The expression of MCP-1<br />
was significantly diminished in COX-2 inhibitor treated rats as compared to untreated<br />
WBN/Kob rats. There was a markedly decreased level of PGE2 and decreased infiltration rate<br />
of macrophages in inhibitor treated rat pancreas. In this study, we investigated the regulation<br />
of pro-inflammatory molecules (PGE2, MCP-1and TNFï¡ © during interactions of pancreatic acinar<br />
cells and macrophages ®<br />
Methods: We first identified the cells which express MCP-1 in the rat model, and found it predominantly<br />
in acinar cells. To simulate interactions of macrophages and acinar cells, we used<br />
a mouse macrophage cell line (RAW 26<strong>4.</strong>7) and a rat acinar cell line (AR42J). To test whether<br />
PGE2 might have any effects in acinar cells we first verified that PGE2 receptors EP1-4 are<br />
actually expressed in AR42J cells. The expression and regulation of MCP-1 in the pancreatic<br />
acinar cell line in response to PGE2 was then examined, and the migration of macrophages<br />
in response to pancreatic acinar secretory products was tested.<br />
Results: Pancreatic acinar cells produced MCP-1, and the expression of MCP-1 was regulated<br />
by TNFï¡ and PGE2. In the presence of PGE2, TNFï¡ dependent expression of MCP-1 was significantly<br />
higher than with TNFï¡ alone (p