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Urokinase-Type Plasminogen Activator Receptor Plays a Role in Neutrophil Migration during Lipopolysaccharide-Induced Peritoneal Inflammation but Not during Escherichia coli—Induced Peritonitis
Ist Teil von
The Journal of infectious diseases, 2006-02, Vol.193 (4), p.522-530
Ort / Verlag
Chicago, IL: The University of Chicago Press
Erscheinungsjahr
2006
Link zum Volltext
Quelle
Oxford Journals 2020 Medicine
Beschreibungen/Notizen
Background. Urokinase-type plasminogen activator receptor (uPAR) is expressed on many different cells, including leukocytes. uPAR has been implicated to playa role in neutrophil migration to sites of inflammation. Methods. To determine the role that uPAR plays in neutrophil recruitment in response to bacterial products or intact bacteria, uPAR gene—deficient (uPAR-/-) and wild-type (wt) mice were injected intraperitoneally with either Escherichia coli or lipopolysaccharide (LPS) derived from this bacterium. Results. uPAR-/- mice demonstrated a decreased LPS-induced neutrophil migration into peritoneal lavage fluid, whereas the chemokine and cytokine response was unaltered. In contrast, during E. coli—induced peritonitis, uPAR-/- mice had a normal neutrophil migration into the primary site of infection. The unaltered neutrophil trafficking in uPAR-/- mice during bacterial infection was corroborated by histological assessment of liver and lung tissue and myeloperoxidase levels in tissue homogenates. uPAR-/- mice displayed slightly but significantly lower bacterial loads in the peritoneal cavity, together with a decreased dissemination to the circulation early during the infection. Conclusion. These data suggest that uPAR, in part, mediates neutrophil migration into the peritoneal cavity on local instillation of LPS but that this function of uPAR can be compensated for during peritonitis caused by intact E. coli.