Macrophage migration inhibitory factor stimulated by Helicobacter pylori increases proliferation of gastric epithelial cells

Autor: Keiji Ogura, Marie Chia Mi Lin, Hsiang-Fu Kung, Annie On-On Chan, Benjamin C.Y. Wong, Douglas E. Berg, Shiu Kum Lam, Harry Hua-Xiang Xia
Jazyk: angličtina
Rok vydání: 2005
Předmět:
Antibodies
Monoclonal - pharmacology
Cell division
In Vitro Techniques
medicine.disease_cause
Monocytes
Microbiology
Helicobacter Infections
Cell Line
Bacterial protein
Bacterial Proteins
Stomach - microbiology - pathology
Antibodies monoclonal
medicine
otorhinolaryngologic diseases
Humans
Monocytes - cytology - microbiology
Helicobacter Infections - pathology
Macrophage Migration-Inhibitory Factors
Mutation
Antigens
Bacterial
biology
Helicobacter pylori
H pylori
Chemistry
Stomach
MIF
Gastroenterology
Antibodies
Monoclonal
Epithelial Cells
General Medicine
PAI
biology.organism_classification
bacterial infections and mycoses
medicine.anatomical_structure
Cell culture
Cell Division - physiology
Cancer research
Macrophage migration inhibitory factor
Helicobacter pylori - genetics
Antigens
Bacterial - genetics
Bacterial Proteins - genetics
Cell Division
Epithelial Cells - metabolism - microbiology - pathology
Macrophage Migration-Inhibitory Factors - immunology - metabolism
Popis: Aim: Helicobacter pylori (H pylori) is associated with increased gastric inflammatory and epithelial expression of macrophage migration inhibitory factor (MIF) and gastric epithelial cell proliferation. This study aimed at determining whether H pylori directly stimulates release of MIF in monocytes, whether the cag pathogenicity island (PAI) is involved for this function, and whether MIF stimulated by H pylori increases gastric epithelial cell proliferation in vitro. Methods: A cytotoxic wild-type H pylori strain (TN2), its three isogenic mutants (TN2Δcag, TN2ΔcagA and TN2ΔcagE) were co-cultured with cells of a human monocyte cell line, THP-1, for 24 h at different organism/cell ratios. MIF in the supernatants was measured by an ELISA. Cells of a human gastric cancer cell line, MKN45, were then co-cultured with the supernatants, with and without monoclonal anti-MIF antibody for 24 h. The cells were further incubated for 12 h after addition of 3H-thymidine, and the levels of incorporation of 3H-thymidine were measured with a liquid scintillation counter. Results: The wild-type strain and the isogenic mutants, TN2ΔcagA and TN2ΔcagE, increased MIF release at organism/cell ratios of 200 /1 and 400/1, but not at the ratios of 50/1 and 100/1. However, the mutant TN2Δcag did not increase the release of MIF at any of the four ratios. 3H-thymidine readings for MKN-45 cells were significantly increased with supernatants derived from the wild-type strain and the mutants TN2ΔcagA and TN2ΔcagE, but not from the mutant TN2Δcag. Moreover, in the presence of monoclonal anti-MIF antibody, the stimulatory effects of the wild-type strain on cell proliferation disappeared. Conclusion: H pylori stimulates MIF release in monocytes, likely through its cag PAI, but not related to cagA or cagE. H pylori-stimulated monocyte culture supernatant increases gastric cell proliferation, which is blocked by anti-MIF antibody, suggesting that MIF plays an important role in H pylori-induced gastric epithelial cell proliferation. © 2005 The WJG Press and Elsevier Inc. All rights reserved.
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Databáze: OpenAIRE
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