Proposed protective mechanism of the pancreas in the rat

Background. heparan sulphate is known to have various functions in the animal body,including surveillance of tissue integrity. administered intraperitoneally,it induces a systemic inflammatory response syndrome and when given locally in the pancreas it initiates a protective inflammatory response. the aim of the present study was to investigate the underlying mechanisms behind cell recruitment following intra-ductal infusion of heparan sulphate. methods. rats were subjected to intraductal-infusion of heparan sulphate,lipopolysaccharide and phosphate buffered saline into the pancreas. pancreatic tissue was harvested 1,3,6,9 or 48 hours after infusion and stained immunohistochemically for myeloperoxidase,ed-1,cinc-1 and mcp-1,as well as using eosin hematoxylin staining. furthermore,mpo activity and mcp-1 and cinc-1 concentrations of tissue homogenates were measured. all differences were analyzed statistically using the mann-whitney u-test. results. during hs infusion,a rapid influx of macrophages/monocytes,as visualized as ed-1 positive cells,was seen reaching a maximum at 6 hours. after 48 hours,the same levels of ed-1 positive cells were noted in the pancreatic tissue,but with different location and morphology. increased neutrophil numbers of heparan sulphate treated animals compared to control could be detected only 9 hours after infusion. the number of neutrophils was lower than the number of ed-1 positive cells. on the contrary,lps infusion caused increased neutrophil numbers to a larger extent than heparan sulphate. furthermore,this accumulation of neutrophils preceded the infiltration of ed-1 positive cells. chemokine expression correlates very well to the cell infiltrate. mcp-1 was evident in the ductal cells of both groups early on. mcp-1 preceded monocyte infiltration in both groups,while the cinc-1 increase was only noticeable in the lps group. conclusions. our data suggest that heparan and lps both induce host defense reactions,though by using different mechanisms of cell-recruitment. this implies that the etiology of pancreatic inflammation may influence how the subsequent events will develop. © 2010 axelsson et al; licensee biomed central ltd.