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Increased production of matrix metalloproteinases in Helicobacter pylori-associated human gastritis.

Artikel i vetenskaplig tidskrift
Författare Philip Bergin
Anders Edebo
Wen Sicheng
Erik Johnsson
Jennie Andersson
Hans Lönroth
Pierre Michetti
Qiang Pan-Hammarström
Marianne Quiding-Järbrink
Publicerad i Helicobacter
Volym 9
Nummer/häfte 3
Sidor 201-10
ISSN 1083-4389
Publiceringsår 2004
Publicerad vid Institutionen för medicinsk mikrobiologi och immunologi
Institutionen för de kirurgiska disciplinerna, Avdelningen för kirurgi
Institutionen för de kirurgiska disciplinerna, Avdelningen för gastroforskning
Sidor 201-10
Språk en
Länkar dx.doi.org/10.1111/j.1083-4389.2004...
Ämnesord Gastric Mucosa, metabolism, microbiology, Gastritis, immunology, microbiology, physiopathology, Helicobacter Infections, immunology, microbiology, physiopathology, Helicobacter pylori, pathogenicity, Humans, Macrophage Activation, Macrophages, immunology, metabolism, Matrix Metalloproteinase 2, metabolism, Matrix Metalloproteinase 9, metabolism, Tissue Inhibitor of Metalloproteinase-1, metabolism, Up-Regulation
Ämneskategorier Immunologi inom det medicinska området

Sammanfattning

BACKGROUND AND AIMS: Helicobacter pylori infection results in an active, chronic inflammation of the gastric mucosa. Previous studies have highlighted the importance of matrix metalloproteinases (MMPs) in diseases involving mucosal inflammation, prompting us to investigate MMP activity in H. pylori-induced gastritis. METHODS: Gastric biopsies were obtained from H. pylori-infected and uninfected volunteers, and MMP activity was assessed using substrate gel electrophoresis. MMP production was also evaluated by immunohistochemistry and real time-polymerase chain reaction. In parallel, tissue inhibitors of MMPs (TIMP) levels and TIMP-MMP complexes were examined in corresponding tissues using enzyme-linked immunosorbent assays and Western blotting. Finally, MMP production by gastric macrophages was determined after stimulation with H. pylori. RESULTS: Antral mucosa of H. pylori-infected subjects demonstrated a 19-fold higher MMP-9 activity than that of uninfected individuals. MMP-2 was present at lower levels, but was also increased in H. pylori-infected individuals, while there was no difference in the total levels of TIMP-1 and TIMP-2 between the groups of volunteers. Significant numbers of MMP-9-containing cells were only found in the H. pylori-infected antral mucosa. Tissue-resident macrophages were significantly increased in H. pylori-infected individuals, and double-staining showed MMP-9 colocalized to macrophages. Furthermore, gastric macrophages secreted MMP-9 in response to H. pylori bacteria. A corresponding 10-fold increase of gene expression of MMP-9 was seen in patients infected with H. pylori compared to uninfected individuals. CONCLUSIONS: Helicobacter pylori infection results in a substantial increase in MMP-9 and MMP-2 activity in the gastric mucosa, probably contributed to in large part by tissue-resident macrophages, while no changes were seen in the TIMP levels. The net increase in gastric MMP activity is likely to contribute to tissue damage during H. pylori-associated gastritis.

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