TY - JOUR
T1 - Urokinase-type plasminogen activator receptor plays a role in neutrophil migration during lipopolysaccharide-induced peritoneal inflammation but not during Escherichia coli-induced peritonitis
AU - Renckens, Rosemarijn
AU - Roelofs, Joris J. T. H.
AU - Florquin, Sandrine
AU - van der Poll, Tom
PY - 2006
Y1 - 2006
N2 - BACKGROUND: Urokinase-type plasminogen activator receptor (uPAR) is expressed on many different cells, including leukocytes. uPAR has been implicated to play a 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
AB - BACKGROUND: Urokinase-type plasminogen activator receptor (uPAR) is expressed on many different cells, including leukocytes. uPAR has been implicated to play a 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
U2 - https://doi.org/10.1086/499601
DO - https://doi.org/10.1086/499601
M3 - Article
C2 - 16425131
SN - 0022-1899
VL - 193
SP - 522
EP - 530
JO - Journal of infectious diseases
JF - Journal of infectious diseases
IS - 4
ER -