Role of complement-derived and bacterial formylpeptide chemotactic factors in the in vivo migration of neutrophils in experimental Escherichia coli pyelonephritis in rats
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State: Public
Version: Final published version
License: Not specified
It was possible to publish this article open access thanks to a Swiss National Licence with the publisher.
State: Public
Version: Final published version
License: Not specified
It was possible to publish this article open access thanks to a Swiss National Licence with the publisher.
Serval ID
serval:BIB_657821773479
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Role of complement-derived and bacterial formylpeptide chemotactic factors in the in vivo migration of neutrophils in experimental Escherichia coli pyelonephritis in rats
Journal
Journal of Infectious Diseases
ISSN
0022-1899 (Print)
Publication state
Published
Issued date
05/1989
Volume
159
Number
5
Pages
959-65
Language
english
Notes
Journal Article
Research Support, Non-U.S. Gov't --- Old month value: May
Research Support, Non-U.S. Gov't --- Old month value: May
Abstract
In experimental Escherichia coli pyelonephritis, the bacterial multiplication in the kidney parenchyma triggers a burst of neutrophil extravascular migration, as measured by the myeloperoxidase (MPO) activity in the kidney, a marker for tissue neutrophil infiltration. To test the mechanisms of in vivo neutrophil migration, pyelonephritis was surgically induced in rats that were then either complement-depleted with cobra venom factor (CVF), resulting in a profound hypocomplementemia for 72 h after inoculation, or treated with phenylbutazone (PB), a competitive antagonist of bacterial chemotactic formylpeptides. Compared to controls, CVF- and PB-treated animals killed when the neutrophil infiltration started (32 h) had a significantly reduced neutrophil infiltration, as measured by kidney MPO activity. This effect disappeared in animals killed 72 h after surgery, when neutrophil infiltration peaked. These data suggest that redundant chemotactic mechanisms triggered neutrophil migration. Inhibiting one of these mechanisms only transiently delayed neutrophil migration but did not affect the peak infiltration.
Keywords
Animals
Cell Migration Inhibition
Cell Movement
Chemotactic Factors/*immunology
Cobra Venoms
Complement C3/immunology
Complement C5/immunology
Escherichia coli Infections/*immunology
Kidney/enzymology
Neutrophils/*immunology
Peroxidase/analysis
Pyelonephritis/*immunology
Random Allocation
Rats
Pubmed
Web of science
Open Access
Yes
Create date
25/01/2008 15:33
Last modification date
14/02/2022 8:55