Bacterial colonization and healing of gastric ulcers: the effects of epidermal growth factor

2000 ◽  
Vol 278 (1) ◽  
pp. G105-G112 ◽  
Author(s):  
Susan N. Elliott ◽  
J. L. Wallace ◽  
W. McKnight ◽  
D. G. Gall ◽  
J. A. Hardin ◽  
...  
Keyword(s):  
Gastric Ulcer ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Ulcer Healing ◽  
Bacterial Colonization ◽  
Neutrophil Infiltration ◽  
Gastric Ulcers ◽  
Gastric Ulcer Healing ◽  
Epidermal Growth

.—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.

Epidermal growth factor (EGF) accelerates experimental gastric ulcer healing by decreasing bacterial colonization

1998 ◽  
Vol 114 ◽  
pp. A113
Author(s):  
S.N. Elliott ◽  
W. McKnight ◽  
J.A. Hardin ◽  
M.E. Olson ◽  
D.G. Gall ◽  
...  
Keyword(s):  
Gastric Ulcer ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Ulcer Healing ◽  
Bacterial Colonization ◽  
Experimental Gastric Ulcer ◽  
Gastric Ulcer Healing ◽  
Epidermal Growth

Increased expression of epidermal growth factor receptor during gastric ulcer healing in rats

1992 ◽  
Vol 102 (2) ◽  
pp. 695-698 ◽  
Author(s):  
Andrzej Tarnawski ◽  
Jerzy Stachura ◽  
Theodore Durbin ◽  
I.James Sarfeh ◽  
Hella Gergely
Keyword(s):  
Epidermal Growth Factor Receptor ◽  
Gastric Ulcer ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Ulcer Healing ◽  
Growth Factor Receptor ◽  
Gastric Ulcer Healing ◽  
Epidermal Growth

Topical transplantation of mesenchymal stem cells accelerates gastric ulcer healing in rats

2008 ◽  
Vol 294 (3) ◽  
pp. G778-G786 ◽  
Author(s):  
Yujiro Hayashi ◽  
Shingo Tsuji ◽  
Masahiko Tsujii ◽  
Tsutomu Nishida ◽  
Shuji Ishii ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Gastric Ulcer ◽  
Growth Factor ◽  
Ulcer Healing ◽  
Gastric Wall ◽  
Female Rats ◽  
Male Rats ◽  
Gastric Ulcers ◽  
Gastric Ulcer Healing

Mesenchymal stem cells (MSCs), a subpopulation of adult somatic stem cells, are an attractive stem cell source in regenerative medicine because of their multipotentiality. We examined the effects of MSC transplantation on gastric ulcer healing. Putative MSCs, isolated from bone marrow aspirates of male rats by dish adherence and expanded in culture, were characterized by flow cytometry and reverse transcription-polymerase chain reaction. Gastric ulcers were induced by serosal application of acetic acid on the anterior wall of the stomach in female rats. Either MSCs (labeled with PKH67; 1×107 cells) or vehicle was injected into the gastric wall surrounding the ulcer. The healing process of the ulcer and the influence of anti-vascular endothelial growth factor (VEGF) antibody were examined. CD29-positive, CD90-positive, CD34-negative, and CD45-negative MSCs expressed mRNAs for VEGF and hepatocyte growth factor (HGF). The MSCs were transplantable to the gastric tissue surrounding the ulcer, where a majority of the engrafted cells were positive for vimentin. The transplantation significantly accelerated gastric ulcer healing compared with controls. The engrafted MSCs also expressed VEGF and HGF. Administration of anti-VEGF neutralizing antibody dose dependently reduced the MSC-induced promotion of ulcer healing. In conclusion, MSC transplantation accelerated gastric ulcer healing, possibly through the induction of angiogenesis in the gastric mucosa via the secretion of VEGF. The beneficial effects of MSCs might be mediated not only by their differentiation into gastric interstitial cells, but also by their ability to supply angiogenic factors.

scholarly journals Effects of Orally Administered Epidermal Growth Factor on Enteropathogenic Escherichia coli Infection in Rabbits

1998 ◽  
Vol 66 (10) ◽  
pp. 4917-4923 ◽  
Author(s):  
Andre Buret ◽  
Merle E. Olson ◽  
D. Grant Gall ◽  
James A. Hardin
Keyword(s):  
Escherichia Coli ◽  
Weight Gain ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Brush Border ◽  
Bacterial Colonization ◽  
E Coli ◽  
Epidermal Growth

ABSTRACT The increased intestinal absorption induced by epidermal growth factor (EGF) is associated with diffuse lengthening of brush border microvilli. The aim of this study was to examine the in vivo effects of oral administration of EGF during infection with enteropathogenicEscherichia coli. New Zealand White rabbits (4 weeks old) received orogastric EGF daily starting 3 days prior to infection with enteropathogenic E. coli RDEC-1 and were compared with sham-treated infected animals and uninfected controls. Weight gain, food intake, fecal E. coli, and stool consistency were assessed daily. On day 10, segments of jejunum, ileum, proximal, and distal colon were assessed for gram-negative bacterial colonization, disaccharidase activities, and epithelial ultrastructure. Effects of EGF on E. coli RDEC-1 proliferation were studied in vitro.E. coli RDEC-1 caused diarrhea and reduced weight gain. Seven days postinfection, the small and large intestines were colonized with numerous bacteria, brush border microvilli were disrupted, and maltase and sucrase activities were significantly reduced in the jejunum. Daily treatment with EGF prevented the occurrence of diarrhea and reduction of weight gain. These effects were associated with significant inhibition of E. coli colonization in the small and large intestine, improved jejunal maltase and sucrase activities and reduced microvillous injury. EGF did not affect the proliferation of E. coli in vitro. The findings suggest that EGF protects the gastrointestinal tract against colonization by enteropathogenicE. coli.

THE EFFECT OF EPIDERMAL GROWTH FACTOR ON QUALITY OF BOVINE OOCYTES AGED IN VITRO

2018 ◽  
pp. 29-33
Author(s):  
G. SINGINA ◽  
◽  
E. SHEDOVA ◽  
I. LEBEDEVA ◽  
◽  
...  
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Epidermal Growth ◽  
Bovine Oocytes

Computational Evaluation and In Vitro Validation of New Epidermal Growth Factor Receptor Inhibitors

2020 ◽  
Vol 20 (18) ◽  
pp. 1628-1639
Author(s):  
Sergi Gómez-Ganau ◽  
Josefa Castillo ◽  
Andrés Cervantes ◽  
Jesus Vicente de Julián-Ortiz ◽  
Rafael Gozalbes
Keyword(s):  
Cell Proliferation ◽  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Binding Affinity ◽  
Cell Lines ◽  
Growth Factor Receptor ◽  
Significant Activity ◽  
Epidermal Growth

Background: The Epidermal Growth Factor Receptor (EGFR) is a transmembrane protein that acts as a receptor of extracellular protein ligands of the epidermal growth factor (EGF/ErbB) family. It has been shown that EGFR is overexpressed by many tumours and correlates with poor prognosis. Therefore, EGFR can be considered as a very interesting therapeutic target for the treatment of a large variety of cancers such as lung, ovarian, endometrial, gastric, bladder and breast cancers, cervical adenocarcinoma, malignant melanoma and glioblastoma. Methods: We have followed a structure-based virtual screening (SBVS) procedure with a library composed of several commercial collections of chemicals (615,462 compounds in total) and the 3D structure of EGFR obtained from the Protein Data Bank (PDB code: 1M17). The docking results from this campaign were then ranked according to the theoretical binding affinity of these molecules to EGFR, and compared with the binding affinity of erlotinib, a well-known EGFR inhibitor. A total of 23 top-rated commercial compounds displaying potential binding affinities similar or even better than erlotinib were selected for experimental evaluation. In vitro assays in different cell lines were performed. A preliminary test was carried out with a simple and standard quick cell proliferation assay kit, and six compounds showed significant activity when compared to positive control. Then, viability and cell proliferation of these compounds were further tested using a protocol based on propidium iodide (PI) and flow cytometry in HCT116, Caco-2 and H358 cell lines. Results: The whole six compounds displayed good effects when compared with erlotinib at 30 μM. When reducing the concentration to 10μM, the activity of the 6 compounds depends on the cell line used: the six compounds showed inhibitory activity with HCT116, two compounds showed inhibition with Caco-2, and three compounds showed inhibitory effects with H358. At 2 μM, one compound showed inhibiting effects close to those from erlotinib. Conclusion: Therefore, these compounds could be considered as potential primary hits, acting as promising starting points to expand the therapeutic options against a wide range of cancers.

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