Bacterial colonization and healing of gastric ulcers: the effects of epidermal growth factor
Autor: | Susan N. Elliott, Webb McKnight, Merle E. Olson, Andre G. Buret, D. G. Gall, James A. Hardin, John L. Wallace |
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Rok vydání: | 2000 |
Předmět: |
Male
Physiology medicine.drug_class Antibiotics Colony Count Microbial Administration Oral Microbiology Gastric Acid Intestinal mucosa Epidermal growth factor Physiology (medical) medicine Animals Colonization Stomach Ulcer Rats Wistar Peroxidase Wound Healing Bacteria Epidermal Growth Factor Hepatology biology Stomach Gastroenterology digestive system diseases Rats Microscopy Electron medicine.anatomical_structure Myeloperoxidase Immunology biology.protein Gastric acid Wound healing hormones hormone substitutes and hormone antagonists |
Zdroj: | American Journal of Physiology-Gastrointestinal and Liver Physiology. 278:G105-G112 |
ISSN: | 1522-1547 0193-1857 |
DOI: | 10.1152/ajpgi.2000.278.1.g105 |
Popis: | —Experimental gastric ulcers are rapidly colonized by various bacteria, resulting in significantly impaired healing. Epidermal growth factor (EGF) is capable of preventing bacterial colonization of the healthy intestinal mucosa. In this study, we examined the possibility that EGF accelerates gastric ulcer healing by reducing bacterial colonization of the ulcer. Gastric ulcers were induced by serosal application of acetic acid. The effect of daily administration of EGF on ulcer healing and bacterial colonization was assessed and compared with the effect of daily treatment with broad-spectrum antibiotics. EGF administration reduced colonization levels and accelerated ulcer healing as effectively as the antibiotic treatment. EGF was without effect on acid secretion or neutrophil infiltration into the ulcer. Bacterial growth was not inhibited in the presence of EGF in vitro. These results demonstrate that EGF reduces bacterial colonization during an established infection of a compromised mucosal surface. This effect may contribute to the ability of EGF to accelerate gastric ulcer healing. This effect is acid independent and not due to an anti-inflammatory effect or to direct bactericidal actions. |
Databáze: | OpenAIRE |
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