Biomarkers in Patients with Gastric Inflammation: A Systematic Review

Abstract

Background: The importance of examining the status of gastric inflammation has been acknowledged; the new classification by the updated Sydney system (USS) allows us to evaluate the quantitative status of gastric inflammation. However, this system is based on the histological classification derived from biopsy specimens. Therefore, more convenient, objective and practical biomarkers are recommended. Aim: We undertook a systematic review to find out potential biomarkers by summarizing the relationship between biomarkers and grades of inflammation. Methods: By a primary search via Medline up to December 2004, we extracted a total of 6,526 papers that described biomarkers for human gastric inflammation. All papers were screened by title and abstract. The authors then retrieved 435 citations for complete review; ultimately 231 were appropriate for inclusion criteria. These papers were subclassified into several categories and summarized by each author. Results: In addition to standard markers such as pepsinogens, we confirmed the close relationship between the levels of several biomarkers including gastrin, interleukin-8, HLA class II molecules, reactive oxygen species, and the histological grades. Conclusions: This review provides valuable information describing the clinical implication of these biomarkers for evaluating the static conditions or dynamic alterations of human gastric inflammation.

Bile Acid Promotes Intestinal Metaplasia and Gastric Carcinogenesis

“…As is well known, IL-8 is a key cytokine that enhances H. pyloriinduced gastric inflammation showing mononuclear cell/neutrophil infiltration in the mucosal layer (28). We showed the possibility that bile acid first has an inhibitory effect on CINC1 expression induced by H. pylori infection, and second, inhibits the infiltration of inflammatory cells in the gastric mucosa.…”

Effect of H. pylori infection on gastrin, ghrelin, motilin, and gastroesophageal reflux

“…In our study, we observed neither a change in the gastrin level nor in GERD occurrence between H. pylori-infected and non-infected state. In contrast to these hypotheses, we could not demonstrate any relationship between gastrin and GERD, which was comparable with a few studies in the literature (18)(19)(20)(21)(22)(23)(24). One of the reasons for this difference can be the predominant corpoantral infection in our patients.…”

The C-Terminal Disulfide Bonds of Helicobacter pylori GroES Are Critical for IL-8 Secretion via the TLR4-Dependent Pathway in Gastric Epithelial Cells

“…IL-8 production in the gastric mucosa has been shown to be induced by H. pylori infection and to correlate with the development of chronic gastritis (16). IL-8 production is also recognized as an early response to H. pylori by the gastric epithelium (14).…”

“…Among these cytokines, IL-8 is the most highly expressed gene in H. pylori-infected gastric epithelial cells and appears to play a major role in the epithelial cell response to H. pylori infection and in the pathological processes leading to gastric disease (14,15). Several studies have demonstrated increased IL-8 production and secretion in response to H. pylori both in vivo and in vitro (16,17). Gastric mucosal IL-8 levels show a positive correlation with the degree of stomach corpus inflammation, and IL-8 expression is also highly increased in gastric cancer (18,19).…”

“…The increased production and secretion of proinflammatory cytokines induced by HpGroES has been shown to contribute to gastric inflammation (7,16,34). However, the molecular mechanism of proinflammatory cytokine induction has not been elucidated.…”