MUC1 and MUC5AC Acting on Helicobacter pylori-Related Deficiency and Solid Syndrome of Spleen and Stomach.

Ling Hu,Ting Zhang,Peiwu Li,Wanqun Chen,Weijing Chen,Shaoyang Lan,Ming Cheng

doi:10.1155/2018/9761919

Abstract

To investigate the relationship of MUC1, MUC5AC, and the syndrome of spleen and stomach, 109 subjects (34 peptic ulcer (PU), 62 chronic gastritis (CG), and 13 healthy volunteers (CON)) were included. All the subjects included were surveyed with questionnaire to classify them into damp-heat syndrome of spleen and stomach (DHSS), spleen-qi deficiency syndrome (SQD), and CON, examined by gastric endoscope, and biopsied. Rapid urease and methylene blue staining (MBS) were performed on every subject to diagnose for Helicobacter pylori (Hp) infection, and both were defined as Hp-positive. Hematoxylin and eosin (HE) staining was performed on every specimen to explore the histomorphology, inflammatory degree, and inflammatory activity of different groups; then Elivision™ plus kit was used to test the expression of MUC1 and MUC5AC. All the results of digital images were reviewed by two experts blindly. The inflammatory degree with Hp infection was higher than those uninfected or CON, but no significant difference was found between DHSS and SQD. And the expressions of MUC5AC with positive Hp was higher than those with negative Hp or CON regardless of the deficiency and solid syndrome of spleen-stomach but not for MUC1. We speculate that the deficiency and solid syndrome of spleen-stomach is a condition like Tai Ji symbol of dynamic equilibrium, showing the higher expression of MUC5AC but no change of MUC1 in the circumstance of Hp infection.

Highlights

It is well established that Helicobacter pylori (Hp) is the main etiologic factor in a range of pathologies including chronic gastritis (CG), peptic ulcer (PU), and even gastric cancer (GC) [1, 2]
The theory that intestine GC is a multistep process starting with CG and progressing through atrophy, intestinal metaplasia (IM), and dysplasia triggered by Hp is well known [3]
On one hand, based on the in vitro and mouse model research, studies have elucidated that Hp dwelling exerts the reduction of MUC1 expression due to the mucosal barrier injury [9,10,11], whereas, on the other hand, it was suggested that glycan-rich niche produced by mucins provides a preferential binding point for Hp [9]; notably, the abnormal expression of MUC1 was recognized as oncogene in the development of gastric carcinomas [12, 13]

Summary

Introduction

It is well established that Helicobacter pylori (Hp) is the main etiologic factor in a range of pathologies including chronic gastritis (CG), peptic ulcer (PU), and even gastric cancer (GC) [1, 2]. MUC1 and MUC5AC are believed to be the most critical proteins for protection from Hp or in the process of carcinogenesis, which have previously been assumed. On one hand, based on the in vitro and mouse model research, studies have elucidated that Hp dwelling exerts the reduction of MUC1 expression due to the mucosal barrier injury [9,10,11], whereas, on the other hand, it was suggested that glycan-rich niche produced by mucins provides a preferential binding point for Hp [9]; notably, the abnormal expression of MUC1 was recognized as oncogene in the development of gastric carcinomas [12, 13]. As the critical mucin and the major receptor for Hp, the dual role of MUC1 and MUC5AC can be considered as powerful twoedged sword

Methods

Results

Conclusion