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, 19 (4), 323-33

Helicobacter Pylori: I. Ultrastructural Sequences of Adherence, Attachment, and Penetration Into the Gastric Mucosa

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Helicobacter Pylori: I. Ultrastructural Sequences of Adherence, Attachment, and Penetration Into the Gastric Mucosa

S M el-Shoura. Ultrastruct Pathol.

Abstract

New ultrastructural observations on the sequences of adherence, attachment, and penetration of Helicobacter pylori (HP) into the gastric epithelium were described in 32 endoscopic biopsies selected randomly from 168 samples of patients with active chronic gastritis. The adherence of HP to the target cell was initiated by direct contact with the microvillar coat, or glycocalyx, leading to the loss of that coat. The next 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 contact with the uncoated cell membrane and are ready for firm attachment. The attachment process was enhanced by the appearance of HP fibrillarlike strands (FLS). Up to three sites of attachment were recognized for individual organisms. Penetration into the apical cytoplasmic regions occurred by one of the organism's poles without damaging the host cell membrane. While a cell is being penetrated by one pole, FLS may extend from the other free pole to be in direct contact with the limiting 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 neutrophils were found penetrating into the base of the gastric glands from 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 granular contents in the gastric lumena play important roles in the gastric lesions during active chronic gastritis.

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