IMMUNOGLOBULIN LEVELS IN TWO DIFFERENT MODELS OF EXPERIMENTAL ACUTE PANCREATITIS

Abstract

Background: While it is known that the expression of many genes in the pancreas is altered in acute pancreatitis, the role of the humoral immune system in acute pancreatitis is not well established. Since immunoglobulins are differentially regulated in inflammatory states, we investigated their presence as a marker in two different models of experimental acute pancreatitis, sodium taurocholate (NaT) and caerulein injection, which induce necrotizing or edematous pancreatitis, respectively. Methods: Acute pancreatitis was induced in Wistar rats by retrograde infusion of either 4% sodium taurocholate (NaT) into the pancreatic duct or serial intraperitoneal injection (IP) of caerulein. After 24 hr, pancreata were harvested and assessed for worsening pancreatitis by histopathology and serum/plasma was collected and analyzed for IgM, IgG, IgA and IgE (ELISA). Data are presented as mean ± SEM, p < 0.05, Student's t-test. Results: Induction of pancreatitis was confirmed by histopathology. Serum IgM and IgG levels were significantly elevated in caerulein pancreatitis (85 ± 10 ug/ml, and 7 ± 0.3 mg/ml respectively) but not in NaT induced pancreatitis (22 ± 2.8 ug/ml, 0.86 ± 0.2 mg/ml, respectively) when compared with controls (healthy rats) (p < 0.05). In contrast, serum IgA levels were significantly elevated in NaT induced pancreatitis (87 ± 36 ug/ml) but not in caerulein induced pancreatitis (20 ± 2.5 ug/ml) when compared with controls (p < 0.05). Serum IgE levels did not differ among groups. Conclusions: Serum immunoglobulin levels are differentially induced in different models of experimental (necrotizing vs. edematous) acute pancreatitis. These insults may provoke different immunoglobulin processing pathways, the study of which may serve to better understand inflammatory pathways and provide diagnostic/prognostic markers in acute pancreatitis.