{'fraction_non_alphanumeric': 0.0136986301369863, 'fraction_numerical': 0.0, 'mean_word_length': 6.349112426035503, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
[Interactions between microbes and enterocytes in experimental intestinal infections].

All enteropathogens first attach to the glycocalyx on the enterocyte surface. Then noninvasive cholera vibrios and enterotoxicogenic E. coli multiply on the enterocyte microvilli producing enterotoxins which cause pronounced enterocyte hypersecretion. Invasive enteropathogens differ in the model of penetration into enterocytes, multiplication site, the effect on the fate of invaded enterocytes, the ability of the infectious process for generalization. Recent studies have confirmed the decisive role of Shigella intraepithelial multiplication in the development of ulcerative dysenteric mucosal inflammation, Salmonella penetration through the enterocytes, multiplication in macrophages and development of not only enterocolitis but generalized infection as well. In case of enteropathogenic E. coli causing infantile enteritis, multiplication of the attached germs with the resulting damage to the enterocyte surface plays the main role whereas bacterial invasion through the enterocytes is limited and of secondary importance. All the invasive enterobacteria produce peculiar cytotoxic enterotoxins which stimulate but also damage the enterocytes.