Complement-induced impairment of innate immunity during sepsis.
J Immunol
; 169(6): 3223-31, 2002 Sep 15.
Article
em En
| MEDLINE
| ID: mdl-12218141
ABSTRACT
This study defines the molecular basis for defects in innate immunity involving neutrophils during cecal ligation/puncture (CLP)-induced sepsis in rats. Blood neutrophils from CLP rats demonstrated defective phagocytosis and defective assembly of NADPH oxidase, the latter being due to the inability of p47(phox) to translocate from the cytosol to the cell membrane of neutrophils after cell stimulation by phorbol ester (PMA). The appearance of these defects was prevented by in vivo blockade of C5a in CLP rats. In vitro exposure of neutrophils to C5a led to reduced surface expression of C5aR and defective assembly of NADPH oxidase, as defined by failure in phosphorylation of p47(phox) and its translocation to the cell membrane, together with failure in phosphorylation of p42/p44 mitogen-activated protein kinases. These data identify a molecular basis for defective innate immunity involving neutrophils during sepsis.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Complemento C5a
/
Explosão Respiratória
/
Sepse
/
Neutrófilos
Tipo de estudo:
Prognostic_studies
Idioma:
En
Revista:
J Immunol
Ano de publicação:
2002
Tipo de documento:
Article
País de afiliação:
Estados Unidos