Inactivation of CD11b in a mouse transgenic model protects against sepsis-induced lung PMN infiltration and vascular injury

Physiological Genomics

Volumn 21, Issue , 2005, Pages 230-242

  Gao, Xiao Pei ^a   Liu, Qinghui ^a   Broman, Michael ^a   Predescu, Dan ^a   Frey, Randall S ^a   Malik, Asrar B ^a  

^a UNIVERSITY OF ILLINOIS   (United States)

Author keywords

CD11B CD18 integrin; Neutrophil function; Neutrophil inhibitory factor; NIF+ + mice; Polymorphonuclear leukocyte; Sepsis induced lung injury

Indexed keywords

BETA2 INTEGRIN; CD11B ANTIGEN; LIPOPOLYSACCHARIDE; LYMPHOCYTE FUNCTION ASSOCIATED ANTIGEN 1; MONOCLONAL ANTIBODY; MONOCLONAL ANTIBODY CD11A; NEUTROPHIL INHIBITORY FACTOR; OXIDIZING AGENT; UNCLASSIFIED DRUG;

ACUTE LUNG INJURY; ANIMAL CELL; ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ANTIGEN BINDING; ANTIGEN EXPRESSION; ARTICLE; BLOOD VESSEL INJURY; BLOOD VESSEL PERMEABILITY; CELL ADHESION; CELL FUNCTION; CONTROLLED STUDY; EDEMA; ENDOTHELIUM CELL; ESCHERICHIA COLI; EXTRAVASATION; IMMUNOPRECIPITATION; IN VIVO STUDY; LUNG INFILTRATE; LUNG SEQUESTRATION; MICROVASCULATURE; MOUSE; NEUTROPHIL; NEUTROPHIL CHEMOTAXIS; NONHUMAN; PRIORITY JOURNAL; PROTEIN EXPRESSION; SEPTICEMIA; TRANSGENIC MOUSE;

ESCHERICHIA COLI; NEGIBACTERIA;

EID: 21244434677     PISSN: 15312267     EISSN: None     Source Type: Journal    
DOI: 10.1152/physiolgenomics.00291.2004     Document Type: Article

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