HELICOBACTER-PYLORI .1. ULTRASTRUCTURAL SEQUENCES OF ADHERENCE, ATTACHMENT, AND PENETRATION INTO THE GASTRIC-MUCOSA

Authors
Citation
Sm. Elshoura, HELICOBACTER-PYLORI .1. ULTRASTRUCTURAL SEQUENCES OF ADHERENCE, ATTACHMENT, AND PENETRATION INTO THE GASTRIC-MUCOSA, Ultrastructural pathology, 19(4), 1995, pp. 323-333
Citations number
32
Categorie Soggetti
Microscopy,Pathology
Journal title
ISSN journal
01913123
Volume
19
Issue
4
Year of publication
1995
Pages
323 - 333
Database
ISI
SICI code
0191-3123(1995)19:4<323:H.USOA>2.0.ZU;2-S
Abstract
New ultrastructural observations on the sequences of adherence, attach ment, and penetration of Helicobacter pylori (HP) into the gastric epi thelium were described in 32 endoscopic biopsies selected randomly fro m 168 samples of patients with active chronic gastritis. The adherence of HP to the target cell was initiated by direct contact with the mic rovillar coat, or glycocalyx, leading to the loss of that coat. The ne xt step was demolishing of the surface microvilli, which separate the organisms from the cell cytoplasmic apices containing the main target of the HP, the mucoid granules. Thus the organisms come into close con tact with the uncoated cell membrane and are ready for firm attachment . The attachment process was enhanced by the appearance of HP fibrilla rlike strands (FLS). Up to three sites of attachment were recognized f or individual organisms. Penetration into the apical cytoplasmic regio ns occurred by one of the organism's poles without damaging the host c ell membrane. While a cell is being penetrated by one pole, FLS may ex tend from the other free pole to be in direct contact with the limitin g membranes of the neighboring cell mucoid granules. Penetration into the gastric cells by a great number of organisms leads to serious cell damage and ultimately to cell disintegration. As a response, many neu trophils were found penetrating into the base of the gastric glands fr om the surrounding lamina propria; these cells were found damaged and disintegrated in the gland lumena. The neutrophils were absolutely HP- nonphagocytic. This study suggests that the dynamic activity of HP in the gastric epithelium and the possible release of the neutrophil gran ular contents in the gastric lumena play important roles in the gastri c lesions during active chronic gastritis.