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Dangerous Liaison: Helicobacter pylori, Ganglionitis, and Myenteric Gastric Neurons: A Histopathological Study - PubMed

  • ️Tue Jan 01 2019

Observational Study

. 2019 Dec 30:2019:3085181.

doi: 10.1155/2019/3085181. eCollection 2019.

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Observational Study

Dangerous Liaison: Helicobacter pylori, Ganglionitis, and Myenteric Gastric Neurons: A Histopathological Study

Liana Sticlaru et al. Anal Cell Pathol (Amst). 2019.

Abstract

Chronic inflammation induced by Helicobacter pylori (H. pylori) infection plays a major role in development of gastric cancer. However, recent findings suggested that progression of inflammation and neoplastic transformation in H. pylori infection are more complex than previously believed and could involve different factors that modulate gastric microenvironment and influence host-pathogen interaction. Among these factors, gastric myenteric plexus and its potential adaptive changes in H. pylori infection received little attention. This study is aimed at identifying the impact of H. pylori-associated gastritis on number and morphology of nerve cells in the stomach. The distribution of density, inflammation, and programmed cell death in neurons was immunohistochemically assessed in full-thickness archival tissue samples obtained from 40 patients with H. pylori infection who underwent surgery for gastric cancer and were compared with findings on samples collected from 40 age- and sex-matched subjects without bacteria. Overall, significant differences were noted between H. pylori-positive and H. pylori-negative patients. The analysis of tissue specimens obtained from those with infection revealed higher density and larger surface of the myenteric nervous plexus, as well as a significant increase in the number of gastric neuronal cell bodies and glial cells compared to controls. A predominant CD3-immunoreactive T cell infiltrate confined to the myenteric plexus was observed in infected subjects. The presence of mature B lymphocytes, plasma cells, and eosinophils was also noted, but to a lesser extent, within the ganglia. Myenteric ganglionitis was associated with degeneration and neuronal loss. Our results represent the first histopathological evidence supporting the hypothesis that H. pylori-induced gastric inflammation may induce morphological changes in myenteric gastric ganglia. These findings could help gain understanding of some still unclear aspects of pathogenesis of H. pylori infection, with the possibility of having broader implications for gastric cancer progression.

Copyright © 2019 Liana Sticlaru et al.

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Conflict of interest statement

The authors declare that there are no conflicts of interest regarding the publication of this paper.

Figures

Figure 1
Figure 1

Number and area of myenteric ganglia in the stomach. Representative photomicrographs of S-100 immunostained ganglionic areas in H. pylori-positive patients (a, ×40) and in control patients (b, ×40). Box and whisker plots showing that gastric myenteric ganglia are larger (c, p < 0.01) and they are increased in number (d, p < 0.01) in H. pylori-infected patients, as compared to controls.

Figure 2
Figure 2

Number of gastric myenteric neurons and glial cells. Graphs showing that significant more myenteric neurons (a, p < 0.00001) and glial cells (b, p < 0.00001) were detected in the H. pylori-positive group in comparison to the control group.

Figure 3
Figure 3

Representative photomicrographs showing different types of inflammatory cells around and within the myenteric plexus in H. pylori-infected patients: lymphocytes (a, H&E stain, 400x); lymphocytes and eosinophils (arrows) (b, H&E stain, 400x); T lymphocytes (c, CD3 stain, 400x); B lymphocytes (d, CD20 stain, 400x). In contrast, no inflammatory cell was noted around myenteric ganglia in control patients (e, H&E stain, 400x).

Figure 4
Figure 4

Representative photomicrographs illustrating signs of myenteric neuronal degeneration in H. pylori-positive patients: condensed cytoplasm and pyknotic nuclei (a, H&E stain, 400x) and vacuolated cytoplasm (b and c, H&E stain, 400x). Normal neurons are shown by arrowheads (c).

Figure 5
Figure 5

Bcl-2 immunohistochemical labeling of gastric myenteric ganglionic neurons: myenteric neurons with reduced or absent expression of antiapoptotic protein bcl-2 in H. pylori-positive patients (a and b, 400x) and normal bcl-2 expression of neurons in myenteric plexus from a control subject (c, 400x).

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