Akademik Veri Yönetim Sistemi
26. Ulusal Elektron Mikroskobi Kongresi, Eskişehir, Türkiye, 20 - 23 Eylül 2023, sa.15, ss.88
SARS-CoV-2 can infect the respiratory system and other systems. Various organs of the gastrointestinal system are reported as targets of the virus. However, there is not enough data on the stomach. Considering that the stomach is a vulnerable organ to bacterial infections, such as Helicobacter pylori, which may cause precancerous lesions in the long term, the acute and chronic course of SARS-CoV-2 and bacterial infection in the stomach is unclear. This study aimed to evaluate the damage caused by bacterial and SARS-CoV-2 co-infections in the stomach through histopathological and ultrastructural changes. K18-hACEII mice (total n=20), which are transgenic mice with human ACE2 receptor, were divided into four groups as control, SARS-CoV-2 infected, bacteria infected, and virus+bacteria infected. For histopathological evaluation, gastric tissues were stained with Hematoxylin & Eosin and PAS. Immunohistochemistry was used for the demonstration of SARS-CoV-2 by light microscopy, and the Gram staining method was used to detect bacteria. Direct cytopathic effects, verification of pathogens, and fine structural damage in the tissue were investigated in transmission electron microscopic examinations. SARS-CoV-2 was localized on the surface and occasionally in the middle parts of the mucosa. Both grampositive and gram-negative bacterial colonization were detected near the gastric Z line. Although acute damage was more prominent in the SARS-CoV-2 infection group, mucosal damage was observed in the stomach in all groups infected with bacteria or virus. Inflammation, erythrocyte extravasation, and focal necrotic areas were observed, especially in the co-infected group. The electron microscopic and light microscopic findings were consistent. In conclusion, viral and bacterial coinfections worsen epithelial damage. Gastric tissue, which was intact before COVID-19 infection, may become predisposed to post-viral bacterial infections due to virusassociated epithelial damage. Given the nature of Helicobacter pylori, the process of metaplasia may be accelerated in a chronic gastritis patient infected later with SARS-CoV-2. Patients should be monitored for new-onset gastric complaints after COVID-19. This study was funded by Scientific Research Projects Coordination Unit of Istanbul University. Project number: 38713.
Keywords: COVID-19, gastritis, helicobacter pylori, SARS-CoV-2, stomach