Angiotensin II increases host resistance to peritonitis

Citation
K. Rodgers et al., Angiotensin II increases host resistance to peritonitis, CL DIAG LAB, 7(4), 2000, pp. 635-640
Citations number
53
Categorie Soggetti
Immunology
Journal title
CLINICAL AND DIAGNOSTIC LABORATORY IMMUNOLOGY
ISSN journal
1071412X → ACNP
Volume
7
Issue
4
Year of publication
2000
Pages
635 - 640
Database
ISI
SICI code
1071-412X(200007)7:4<635:AIIHRT>2.0.ZU;2-D
Abstract
Studies by other laboratories have shown that angiotensin II (AII) can affe ct the function of cells which comprise the immune system. In the present s tudy, the effect of rin on the function of peritoneal macrophages and perip heral blood monocytes was assessed. In vitro exposure (4 h prior to assay) of peritoneal macrophages from mice and rats to AII increased the percentag e of tells that phagocytosed opsonized yeast and the number of yeast per ma crophage. Furthermore, AII increased the respiratory burst capacity of peri toneal macrophages from mice and rats and peripheral blood mononuclear cell s from humans. Because of these observations, the effect of on host resista nce to bacterial infection was assessed. Intraperitoneal administration of AII was shown to increase host resistance (reduced abscess formation) in an animal model of bacterial peritonitis, Studies were then conducted to asse ss whether parenteral administration of AII, a clinically relevant route, c ould affect peritoneal host resistance in a manner similar to that observed after peritoneal administration. These studies showed that subcutaneous ad ministration of AII throughout the postinfection interval increased the lev el of host resistance to bacterial peritonitis. Furthermore, in a study whi ch compared AII and Neupogen, an agent approved for use for the reduction o f febrile neutropenia after myeloablative therapy, daily subcutaneous admin istration of AII reduced abscess size and incidence, whereas Neupogen did n ot have any therapeutic benefit in this model. These data suggest that AII may be of therapeutic benefit as an immunomodulatory agent.