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Angiotensin II receptor expression and relation to Helicobacter pylori-infection in the stomach of the Mongolian gerbil.

Artikel i vetenskaplig tidskrift
Författare Peter Hallersund
Herbert F Helander
Anna Casselbrant
Anders Edebo
Lars Fändriks
Anders Elfvin
Publicerad i BMC gastroenterology
Volym 10
Nummer/häfte 3
ISSN 1471-230X
Publiceringsår 2010
Publicerad vid Institutionen för kliniska vetenskaper, Avdelningen för gastrokirurgisk forskning och utbildning
Institutionen för kliniska vetenskaper, Avdelningen för pediatrik
Språk en
Länkar dx.doi.org/10.1186/1471-230X-10-3
Ämnesord renin-angiotensin system, stomach, Mongolian gerbil, Helicobacter pylori-infection
Ämneskategorier Fysiologi, Kirurgi

Sammanfattning

BACKGROUND: The role of the renin-angiotensin system in gastric physiology and disease has as yet been sparsely explored. The first aim of the study was to investigate the baseline presence and location of angiotensin II receptors (AT1R and AT2R) in the stomach of the Mongolian gerbil. A second aim was to elucidate whether the presence of H. pylori infection is associated with changes in the expression of these receptors. METHODS: H. pylori-negative and H. pylori-infected (strain SS1 or TN2GF4) male Mongolian gerbils were investigated. The stomachs were examined at six or 12 months after inoculation by the use of immunohistochemistry, western blot and microscopic morphometry. RESULTS: AT1R and AT2R were located in a variety of cells in the gerbil gastric wall, including a subpopulation of endocrine cells in the antral mucosa and inflammatory cells infiltrating H. pylori-infected stomachs. Gerbils infected with the SS1 strain showed a significantly increased antral AT1R protein expression and an increased number of infiltrating polymorphonuclear leucocytes (PMNs) at 12 months. The AT1R protein expression correlated with the number of PMNs and the antral expression of myeloperoxidase. CONCLUSIONS: Angiotensin II receptors are present in a variety of cells in the gastric wall of the Mongolian gerbil. The results indicate an influence dependent on the H. pylori strain on the gastric AT1R expression and a relationship between gastric AT1R expression and mucosal PMNs infiltration.

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