一种用于研究幽门螺杆菌与人胃酸分泌相互作用的模型。

A model for the study of Helicobacter pylori interaction with human gastric acid secretion.

作者信息

Joseph Ian M, Kirschner Denise

机构信息

Department of Microbiology and Immunology, The University of Michigan Medical School, 6730 Medical Science Building II, Ann Arbor, MI 48109-0620, USA.

出版信息

J Theor Biol. 2004 May 7;228(1):55-80. doi: 10.1016/j.jtbi.2003.12.004.

DOI:10.1016/j.jtbi.2003.12.004

PMID:15064083

Abstract

We present a comprehensive mathematical model describing Helicobacter pylori interaction with the human gastric acid secretion system. We use the model to explore host and bacterial conditions that allow persistent infection to develop and be maintained. Our results show that upon colonization, there is a transient period (day 1-20 post-infection) prior to the establishment of persistence. During this period, changes to host gastric physiology occur including elevations in positive effectors of acid secretion (such as gastrin and histamine). This is promoted by reduced somatostatin levels, an inhibitor of acid release. We suggest that these changes comprise compensatory mechanisms aimed at restoring acid to pre-infection levels. We also show that ammonia produced by bacteria sufficiently buffers acid promoting bacteria survival and growth.

摘要

我们提出了一个全面的数学模型，用于描述幽门螺杆菌与人类胃酸分泌系统的相互作用。我们使用该模型来探索允许持续性感染发展并维持的宿主和细菌条件。我们的结果表明，在定植后，在持续性感染建立之前有一个短暂的时期（感染后第1 - 20天）。在此期间，宿主胃部生理发生变化，包括胃酸分泌的正向调节因子（如胃泌素和组胺）升高。这是由胃酸释放抑制剂生长抑素水平降低所促进的。我们认为这些变化包括旨在将胃酸恢复到感染前水平的代偿机制。我们还表明，细菌产生的氨足以缓冲胃酸，促进细菌的存活和生长。