Related Experiment Video
Updated: Jun 13, 2026

Isolation of Cells with Morphological and Spatial Information from Oral Submucous Fibrosis Samples by Laser Capture Microdissection
Published on: August 11, 2023
Lysozyme overexpression in fundic gland polyps
1Gastrointestinal and Liver Pathology Research Laboratory, Department of Pathology, Karolinska Institute and University Hospital, 17176, Stockholm, Sweden. Carlos.Rubio@ki.se
Unlabelled:
Backgroud: Helicobacter pylori (Hp) rarely proliferates in patients with fundic gland polyps (FGPs). We recently found that FGPs express lysozyme, one of the natural defence substances against infection. We aimed to assess the degree of lysozyme expression in a cohort of consecutive FGPs.
Materials And Methods:
A total of 153 gastric biopsies were investigated: 93 with FGPs, 30 with normal mucosa (Nm), 15 with Hp-induced chronic gastritis (Hp-gastritis) and 15 with chronic gastritis without Hp infection (non-Hp-gastritis). Sections were stained with anti-lysozyme (muramidase).
Results:
Lysozyme was slightly to moderately expressed in the surface and foveolar pits, being markedly expressed in the neck glands in Nm, in non-Hp and Hp-gastritis. The ratio of lysozyme neck glands-foveoli was higher in non-Hp than in Nm and even higher in Hp-gastritis. In FGPs, lysozyme was markedly expressed in the surface, the foveolar pits and the cells that partly or entirely covered the microcysts.
Discussion And Conclusion:
While the moderate expansion of the lysozyme-producing cells of the neck glands in Hp-gastritis might be insufficient to eradicate these bacteria, the overproduction of lysozyme in the epithelium covering FGP could be an explanation for the lack of Hp proliferation in these patients.
Insights
Fundic gland polyps (FGPs) show high lysozyme expression, potentially explaining why Helicobacter pylori (Hp) rarely proliferates in these patients. This natural defense mechanism warrants further investigation.
Area of Science:
- Gastroenterology
- Pathology
- Microbiology
Background:
- Helicobacter pylori (Hp) infection is common, but its proliferation is notably rare in patients with fundic gland polyps (FGPs).
- FGPs exhibit expression of lysozyme, a key component of the innate immune system involved in combating microbial infections.
Purpose of the Study:
- To investigate and quantify the expression levels of lysozyme in fundic gland polyps (FGPs).
- To correlate lysozyme expression patterns with the presence or absence of Helicobacter pylori (Hp) infection.
Main Methods:
- Analysis of 153 gastric biopsies, including FGPs, normal mucosa, Hp-induced gastritis, and non-Hp gastritis.
- Immunohistochemical staining using anti-lysozyme (muramidase) antibodies to assess lysozyme distribution and intensity.
Main Results:
- Lysozyme expression was observed in various gastric tissues, with marked expression in neck glands of normal mucosa and gastritis.
- A higher ratio of lysozyme in neck glands compared to foveoli was noted in non-Hp gastritis and Hp-gastritis.
- FGPs demonstrated significant lysozyme expression in surface epithelium, foveolar pits, and cyst-lining cells.
Conclusions:
- The elevated lysozyme production in the epithelium of FGPs may serve as a protective mechanism against Helicobacter pylori proliferation.
- While lysozyme in gastritis may not be sufficient for bacterial eradication, its overproduction in FGPs offers a potential explanation for the low incidence of Hp infection in these polyps.
More Related Videos
04:08Evaluation of the Effectiveness of Longitudinal Incision for Endoscopic Submucosal Excavation of Gastric Subepithelial Lesions
Published on: April 28, 2026
05:57Establishment and Histological Analysis of Esophageal Organoids Modeling the Progression from Normal to Cancerous Tissues
Published on: May 30, 2025
Related Concept Videos
Gastritis-II: Pathophysiology
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
Gastritis II: Pathophysiology
Pleiotropy
Peptic Ulcer Disease II: Pathophysiology
Peptic Ulcer Disease II: Pathophysiology
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.
Peptic Ulcer Disease I: Introduction
An acute ulcer, marked by superficial erosion and minimal inflammation, swiftly resolves upon identifying and addressing the underlying cause. In contrast, a chronic ulcer persists, potentially eroding through the muscular wall and forming fibrous tissue.
Peptic ulcers can also be...