Complement and tumor necrosis factor-alpha contribute to Mac-1 (CD11b/CD18) up-regulation and systemic neutrophil activation during endotoxemia in vivo.

@article{Witthaut1994ComplementAT,
  title={Complement and tumor necrosis factor-alpha contribute to Mac-1 (CD11b/CD18) up-regulation and systemic neutrophil activation during endotoxemia in vivo.},
  author={R Witthaut and Anwar Farhood and Clifton Smith and Helmut Jaeschke},
  journal={Journal of leukocyte biology},
  year={1994},
  volume={55 1},
  pages={105-11}
}
The increased expression of Mac-1 (CD11b/CD18) adhesion glycoproteins on neutrophils was studied using flow cytometry in male Fischer 344 rats treated with 5 mg/kg Salmonella enteritidis endotoxin. A rapid and sustained threefold increase of Mac-1 expression was observed after endotoxin injection. Inhibition of complement activation with the soluble complement receptor type 1 (sCR1) completely suppressed the initial up-regulation of Mac-1 (< or = 15 min) but did not prevent the activation… CONTINUE READING