This book is a comprehensive overview of invited contributions on Helicobacter pylori infection in gastritis and gastric carcinogenesis. The first part of the book covers topics related to the pathophysiology of gastric mucosal defense system and gastritis including the gastroprotective function of the mucus, the capsaicin-sensitive afferent nerves and the oxidative stress pathway involved in inflammation, apoptosis and autophagy in H. pylori related gastritis. The next chapters deal with molecular pathogenesis and treatment, which consider the role of neuroendocrine cells in gastric disease, DNA methylation in H. pylori infection, the role of antioxidants and phytotherapy in gastric disease. The final part presents the effects of cancer risk factors associated with H. pylori infection. These chapters discuss the serum pepsinogen test, K-ras mutations, cell kinetics, and H. pylori lipopolysaccharide, as well as the roles of several bacterial genes (cagA, cagT, vacA and dupA) as virulence factors in gastric cancer, and the gastrokine-1 protein in cancer progression.

This book provides a broad overview of the current understanding of Helicobacter pylori emphasizing its world health impacts. It includes 13 chapters organized into 3 parts: "Pathologies and Treatment", "Host Response" and "Bacterial Defence". Part I (5 chapters) reviews the epidemiology of H. pylori infection, H. pylori infection in Asia, gastric adenocarcinoma, antimicrobial resistance and approaches to treatment, and extragastric manifestations of H. pylori infection. Part II (4 chapters) describes H. pylori-induced acquired immunity and immunoregulation, host genetic factors and susceptibility to H. pylori pathogenesis, innate immune initiators and effectors in H. pylori infection, and H. pylori vaccines. Part III (4 chapters) discusses the importance of H. pylori lipopolysaccharides in gastric adaptation and pathogenesis, H. pylori virulence factors, H. pylori adhesion to the gastric surface, and helicobacteromics. This book is an essential resource for researchers, students and medics in infectious and Helicobacter-associated diseases.

Now that Helicobacter pylori is generally accepted as a key aetiological agent in gastric cancer as well as the main agent in peptic ulcer, it can claim to be the most important new discovery in clinical gastroenterology of the last decade, and yet there is no up-to-date book available on the subject that is designed primarily for the clinical gastroenterologist. This book aims to fill that niche. It should also be of interest to the basic scientist, to those providing a clinical laboratory service (microbiologists and histopathologists), and to epidemiologists and others involved in clinical research.

Helieobaeter pylori has recently been recognized as a new genus according to specific taxonomic criteria; the "popular" name Campylobaeter pylori has been corrected by scientific progress. Following the discovery of the spiral microorgan ism in gastric mucosa by Marshall and Warren in 1982, it took only a few years for H. pylori to become established as a factor in the pathogenesis of gastritis and peptic ulcer disease. Interest in different aspects of H. pylori has grown continuously and has attracted scientists from various medical and biological disciplines such as gastroenterology, microbiology, pathology, immunology, and pharmacology. Indeed H. pylori provides an excellent model for interdisciplinary interaction and cooperation. To promote this concept of interdisciplinary research and exchange of knowledge, a European Campylobacter (Helicobacter) Pylori Study Group was founded in 1987 in Copenhagen. The second meeting of this expanding group was held from October 12-14,1989 in Ulm, FRG. The fact that more than 500 participants attended the conference and that 187 original contributions from all five continents were presented clearly confirmed that H. pylori has "scientifically infected" the whole world. Our understanding of the microbiological and pathogenetic aspects of H. pylori is continuously being challenged as new results follow swifthy from different research areas. This book includes an update and progress report on the various aspects of H. pylori presented and discussed in special workshops held during the meeting in Ulm.

In the rapidly evolving field of Helicobacter infection new data on pathogenetic and pathophysiological mechanism have appeared. New methods which will be more sensitive and specific in the diagnosis of the infection are being developed and in this proceedings the first attempt using PCR technology is published. From the clinical point of view, a challenging aspect that needs clarification, is the observation which suggests an appearance of a correlation between the presence of the bacteria and abdominal pain and other symptoms in children whereas in old age no such correlation is evident. The relationship of H. pylori and gastric cancer is studied with histopathological data and epidemiological approaches. On the treatment side schemes using short courses and new antibiotic combinations are being investigated and preliminary data are reported.

This book is a comprehensive overview of invited contributions on Helicobacter pylori infection in gastritis and gastric carcinogenesis. The first part of the book covers topics related to the pathophysiology of gastric mucosal defense system and gastritis including the gastroprotective function of the mucus, the capsaicin-sensitive afferent nerves and the oxidative stress pathway involved in inflammation, apoptosis and autophagy in H. pylori related gastritis. The next chapters deal with molecular pathogenesis and treatment, which consider the role of neuroendocrine cells in gastric disease, DNA methylation in H. pylori infection, the role of antioxidants and phytotherapy in gastric disease. The final part presents the effects of cancer risk factors associated with H. pylori infection. These chapters discuss the serum pepsinogen test, K-ras mutations, cell kinetics, and H. pylori lipopolysaccharide, as well as the roles of several bacterial genes (cagA, cagT, vacA and dupA) as virulence factors in gastric cancer, and the gastrokine-1 protein in cancer progression.