METABOLOGY OF HELICOBACTER PYLORI INFECTION: ROLE OF GASTROKINES
Wenxiang Wei*, Yanyan Bai*, Anton B. Tonchev1, Ivan S. Stankulov2, and George N. Chaldakov1
* Department of Cellular and Molecular Biology, School of Medicine, Suzhou University, Suzhou, China,
1 Division of Cell Biology and 2 Department of Forensic Medicine and Cell Biology, Medical University, Varna, Bulgaria
Trillions of bacteria, collectively referred to as the microbiota, reside in gastrointestinal tract. Helicobacter (Campylobacter) pylori (H. pylori) is an Gram negative bacillus which infects about half of the world’s population. Its causative role in gastroduodenal disease is well known. Recent studies also implicated H. pylori infection in the pathobiology of autoimmune diseases such as rheumatoid arthritis and idiopathic thrombocytopenic purpura. However, little is known about H. pylori-associated alterations in metabolic pathways and food intake as related to cardiometabolic diseases such as atherosclerosis, obesity, diabetes, and metabolic syndrome. This novel approach is conceptualized as metabology of H. pylori infection. Here we Dance Round this specific topic, with special reference to possible roles played by gastric cell-secreted molecules such as leptin, ghrelin and various cytokines, collectively designated gastrokines. Biomed Rev 2006; 17: 123-128.
Key words: Helicobacter pylori, cardiometabolic disease, cytokines, ghrelin, leptin, metabolism
Received 4 December 2006, received revised 21 December 2006, accepted 23 December 2006. Correspondence and reprint request to Dr George Chaldakov, Division of Cell Biology, Medical University, Varna, Bulgaria. Tel.: 359 52 754 394, Fax: 359 52 650 019,