Introduction:: Intestinal and opportunistic pathogenic bacteria are found in the duodenum; however, pancreas is almost sterile. This is because of the defense mechanisms of biliary tract such as bile flow and the sphincter of Oddi. The sphincter of Oddi is a boundary for bacterial colonization and thus serves as barrier to infiltration [2]; so the sphincter of Oddi dysfunction, observed in chronic pancreatitis, seems to increase infiltration. However, it has been poorly understood how bacterial infiltration is influenced by the sphincter of Oddi function, i.e., periodic contraction. As pancreatic duct is elastic, it is deformed by the changes in the surrounding sphincter's pressure. Deformed duct changes internal fluid flow, which in turn influences bacterial infiltration. The objective is to mathematically model bacterial infiltration in a deformable pancreatic duct.
Materials and Methods:: Pancreatic duct is modeled as an axisymmetric cylinder, attached with a hemisphere for major papilla, with an orifice with 1 mm diameter. Mathematical model included large deformation, fluid flow, and bacterial transport. Large deformation is described in equilibrium equation and stress-strain relationship. For the boundary condition, stress of the outer wall of duct is equal to duodenal fluid pressure, the sphincter of Oddi pressure, and interstitial fluid pressure in the pancreas. The sphincter of Oddi pressure is modeled by including periodic changes over time due to contraction. The effect of propagation of contraction wave in an antegrade or retrograde way is also included. The governing equations are solved using COMSOL Mutiphysics with boundary and initial conditions.
Results, Conclusions, and Discussions:: Simulated structure of the deformed duct is consistent with literature [3]. Moreover, simulated bile distribution in a deforming duct, following the sphincter's contraction, agreed reasonably well with findings in literature [4]. When sphincter of Oddi is being contracted and thus pressure is increasing, bacteria at the duodenum do not infiltrate into the duct. However, the subsequently relaxing sphincter with decreasing pressure allowed bacteria to infiltrate in the expanding duct. The contraction wave following antegrade propagation helps prevent this infiltration by showing peristalsis-like deformation, reducing the reflux fluid velocity. Parametric sensitivity analysis showed bacterial infiltration is increased with thinner wall thickness and greater contraction amplitude and frequency, and retrograde propagation of contraction waves. It has been controversial how the sphincter of Oddi function affects bacterial infiltration to the pancreas; for example, bacterial infiltration is increased in chronic pancreatitis, accompanied with the sphincter of Oddi dysfunction with increased contraction pressure [5]. On the other hand, bacterial infiltration is also increased in the sphincter of Oddi laxity [6]. Increase in the contraction pressure increases bacterial infiltration due to sphincter's pressure decrease, though lower contraction pressure may lead to a decrease in the pancreatic duct pressure. Lower pancreatic duct pressure than duodenal pressure also causes a reflux. Therefore, it seems likely that the periodic contraction of the sphincter of Oddi in healthy individuals is well-balanced to prevent bacterial infiltration.
Acknowledgements (Optional): : This work was supported by Japanese Society of the Promotion of Science, Grants-in-Aid for Early Career Scientists, number 22K18175.
References (Optional): : [1] Geenen et al. (1980). Gastroenterology, 78(2), 317-324. [2] Sung et al. (1990), Microb Ecol Health Dis. 3(4),199-207. [3] Ishibashi et al.(2000). Clin. Anat. 13(3). 159-167. [4] Yokoyama (1986). Jpn.J. Gastroenterol. Surg.19 (6). 1009-1019. [5] Maekawa et al. (2018).Biochem. Biophys. Res. Commun., 506(4), 962-969. [6] Liang et al. (2016). J Am Coll Surg .222(3), 269-280.
