Helicobacter
Dongyou Liu in Handbook of Foodborne Diseases, 2018
H. pylori infection plays a causative role in the development of chronic atrophic gastritis and intestinal metaplasia. Using gastric and intestinal epithelial cell markers, intestinal metaplasia was divided into two major types: a gastric and intestinal mixed type and a solely intestinal type.92,93 In the former, gastric and intestinal phenotypic markers were localized within a glandular level as well as at the same cellular level.94 In Mongolian gerbil model, gastric and intestinal mixed type intestinal metaplasia was found to appear first, followed by the solely intestinal type with appearance of Paneth cells during the overall course of H. pylori infection in the heterotopic proliferative glands.87 It indicated that intestinal metaplasia could be caused by the gradual intestinalization from proper gastric gland cells toward completely intestinal type cells through intermittent gastric and intestinal mixed phenotype.
Helicobacter
Dongyou Liu in Laboratory Models for Foodborne Infections, 2017
H. pylori infection plays a causative role in the development of chronic atrophic gastritis and intestinal metaplasia. Using gastric and intestinal epithelial cell markers, intestinal metaplasia was divided into two major types: a gastric-and-intestinal mixed type and a solely intestinal type.68,69 In the former, gastric and intestinal phenotypic markers are localized within a glandular level as well as in a cellular level.70 In the Mongolian gerbil model, gastric-and-intestinal mixed-type intestinal metaplasia was found to appear first, followed by the solely intestinal type with appearance of Paneth cells during the overall course of H. pylori infection in the HPG.62 It indicated that intestinal metaplasia could be caused by the gradual intestinalization from proper gastric gland cells toward completely intestinal type cells through the intermittent gastric-and-intestinal mixed phenotype.
The gastrointestinal system
C. Simon Herrington in Muir's Textbook of Pathology, 2020
Helicobacter pylori is a spiral bacterium that has become remarkably well adapted to life at the interface between the surface epithelium of the stomach and the covering layer of secreted mucus. The organism causes direct epithelial cell injury, and also excites a vigorous immune response – two mechanisms for developing a chronic inflammatory reaction. Histologically, the mucosa shows a mixed inflammatory cell response with neutrophil infiltration of the epithelium, and a lymphocyte and plasma cell infiltrate in the stroma (this mixed pattern is often referred to as ‘active chronic gastritis’; Figure 10.23). Severe, long-standing epithelial injury may lead to glandular atrophy. The epithelium may also show an adaptive response termed ‘intestinal metaplasia’, in which a partial or almost complete change in epithelial cell differentiation towards small intestinal type occurs. This benefits the host insofar as the intestinal mucosa is resistant to H. pylori infection.
Potential utility of nano-based treatment approaches to address the risk of Helicobacter pylori
Published in Expert Review of Anti-infective Therapy, 2022
Sohaib Khan, Mohamed Sharaf, Ishfaq Ahmed, Tehsin Ullah Khan, Samah Shabana, Muhammad Arif, Syed Shabi Ul Hassan Kazmi, Chenguang Liu
The transmission of H. pylori from person to person can occur through saliva, and it might be spread out through the excrement of food or water, untreated water, poor hygiene, and crowded conditions that largely contribute to the prevalence of H. pylori infection [49]. In brief, it is more likely to be transmitted within the household conditions as it enters the body through the oral cavity and travels to the digestive system, where it infects the stomach or the first part of the small intestine, thereby causing inflammation at the targeted area. The most peculiar characteristic of H. pylori is to survive in the harsh acidic environment of the stomach. It produces urease upon entering the stomach, which then reacts with urea to form ammonia and neutralizes the surrounding environment, consequently leads to the overproduction of the stomach acid (Figure 1) illustrates the invasion of H. pylori infection in the stomach that comprises of six steps; 1) movement of the pathogen through normal stomach lining (mucosa), 2) causing inflammation of the stomach lining (chronic gastritis), 3) loss of stomach cells and weakening of digestive system (atrophic gastritis), 4) transformation of the stomach lining (intestinal metaplasia), 5) initial stages of stomach cancer (dysplasia), and finally cause stomach cancer (gastric adenocarcinoma) [49].
Characteristic analysis of early gastric cancer after Helicobacter pylori eradication: a multicenter retrospective propensity score-matched study
Published in Annals of Medicine, 2023
Xinyuan Liu, Xinyu Wang, Tao Mao, Xiaoyan Yin, Zhi Wei, Jindong Fu, Jie Wu, Xiaoyu Li
The endoscopic and histopathological characteristics of H. pylori infection-related well-differentiated adenocarcinoma are shown in Figure 3. There was a slightly reddish, transverse, patchy mucosa with a rough surface and slight depression in the center, approximately 28 × 18 mm in size on the side of the lesser curvature in the middle of the gastric body (Figure 3(A)). Under NBI, the boundary was clear, and most of the microstructures were caviar-like with dilated microvessels (Figure 3(B)). The glands in the adenocarcinoma area were mainly thick papillary structures covered with atypical epithelium (Figure 3(C)). Tumor cell atypia was remarkable and the nucleocytoplasmic ratio was significantly increased (Figure 3(D)). In the comparison of the two cases, the map-like redness and depressed features of GC after H. pylori eradication were more obvious, which was in line with the endoscopic characteristics. Intestinal metaplasia was observed in both cases and cell atypia was obvious.
Analysis of factors associated with recovery of the serum pepsinogen ratio after Helicobacter pylori eradication: a long-term follow-up study in Korea
Published in Scandinavian Journal of Gastroenterology, 2019
Jun-Hyung Cho, Seong Ran Jeon, So-Young Jin, Suyeon Park
The baseline characteristics of the study population are shown in Table 1. The mean age of the patients was 55.1 (±13.3) years and the proportion of male patients was 53.5%. The mean serum PG I, PG II levels and PG I/II ratio were 74.9 (±40.8) ng/mL, 25.4 (±12.7) ng/mL, and 3.07 (±1.2), respectively. The mean level of serum gastrin was 106.4 (±103.9) pg/mL. According to the degree of gastric atrophy, 156 patients (47.7%) were classified into the none/mild atrophy group, 106 (32.4%) into the moderate atrophy group, and 65 (19.9%) into the severe atrophy group. Intestinal metaplasia was present in 172 patients (52.6%). In terms of H. pylori eradication therapy, 171 patients (52.3%) were treated with the conventional regimen and 156 (47.7%) received a tailored H. pylori eradication regimen based on the results of molecular testing for clarithromycin resistance.
Related Knowledge Centers
- Metaplasia
- Epithelium
- Stomach
- Esophagus
- Gastrointestinal Tract
- Barrett'S Esophagus
- Helicobacter Pylori
- Gastroesophageal Reflux Disease
- Adenocarcinoma
- Small Intestine