Introduction: In the pancreas, aging has been associated with reduced regeneration after resection, and reduced survival after AP. In this study, we investigated the effect of age on severity of AP using biochemical markers, histology and expression of the protective pancreatitis associated proteins (PAPs). Methods: AP was induced via intraductal injection of 4% sodium taurocholate in 3, 12 and 18 month old rats. Animals were stratified to normal, sham and AP groups. Sera and pancreata were assayed at 24hr; statistical significance defined as (*P<0.05). Data is presented as young vs old AP, Mean ±SD, 4-8 animals per group. Results: Compared to young rats, histopathologic scores in older animals after AP had less inflammation (arbitrary scores 7.7±1.3 vs 5.8±1.3*) but unchanged necrosis. While amylase and lipase were mildly depressed in aging, edema significantly decreased and CRP sig increased in the very old group when compared to young (1.52±0.26 vs 1.24±0.07 U/L* and 0.24±0.13 vs 2.4±1.2mg/dL*, respectively). No differences were seen in tissue myeloperoxidase or monocyte-chemotactic-protein1. Older normal rats expressed less pancreatic reg I and PAP 1 mRNAs, and in PAP 1 protein levels were depressed as well when compared to young (10±4 vs 4.7±2.8 x10³ OD, FIGURE); no changes were seen in reg I, PAP2 or 3. Regarding potential antimicrobial activity of PAPs, in AP there was an increase in pancreatic bacteria as measured by PCR of 16S bacterial DNA from the pancreatic tissue. Conclusions: In the older pancreas, Reg I and PAP 1 levels are depressed. After AP, inflammatory infiltrates and biochemical markers are depressed, along with a blunted PAP1 protein response. Older animals have more bacterial infiltration, and more CRP. Since PAPs activate macrophages and bind bacteria, the loss of this protective effect could explain the increased complication rates noted in elderly patients after AP.