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- H El-Adawi, M El-Sheekh, M Khalil, N El-Deeb, and M Hussein.
- Department of Medical Biotechnology, Genetic Engineering and Biotech Institute, Mubarak City for Scientific Research, Universities and Research District Sector, New Borg El-Arab, P.O.BOX 29134, Alexandria, Egypt. halaeladawi@hotmail.com
- Ir J Med Sci. 2013 Sep 1; 182 (3): 439452439-52.
BackgroundHelicobacter pylori (H. pylori) infection, the main cause of chronic gastritis, increases gastric cancer risk. Antibiotics-based H. pylori eradication treatment is 90% effective. However, it is expensive and causes side effects and antibiotic resistance. Lactic acid bacteria (LAB) could present a low-cost, large-scale alternative solution to prevent or decrease H. pylori colonization.AimThis work aimed to study the inhibitory effects of LAB strains on the growth and pathogenic activity of H. pylori stains. To this end, we have selected the most virulent H. pylori strains (out of 20 mucosal antral biopsies) regarding cellular vacuolization and induction of apoptosis/necrosis.MethodThe selection of H. pylori pathogenic strains (clinically pre-isolated) were based on their impact of VacA activities on Hep-2 cell line, induction of apoptosis and necrosis in Caco-2 cell line. The Inhibitory effect of LAB strains on the invasion was carried out using the Caco-2 and Hela cell lines, where, they were co-cultured with the pathogenic H. pylori in the presence or absence of LAB extracts. The effect of LAB extracts on TNF-α secretion which induced by H. pylori-LPS was carried out by RT-qPCR.ResultsL. bulgaricus DSMZ 20080, L. acidophilus and L. plantarum (studied previously and reported as high antioxidant candidate strains) showed the highest anti-pylori activities with inhibition ranged from 51.46 to 88.19%, they preventing the adhesion, invasion and DNA fragmentation of cell lines. In addition, they could reduce the TNF-α expression by 62.13%.ConclusionLAB extracts could inhibit the bacterial adhesion and invasion, gastric inflammation and DNA fragmentation induced by Helicobacter pylori.
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