TITLE

CD64 surface expression on neutrophils is transiently upregulated in patients with septic shock

AUTHOR(S)
Fischer, Guenther; Schneider, Elisabeth; L. Moldawer, Lyle; Karcher, Christian; Barth, Eberhard; Suger-Wiedeck, Heidemarie; Georgieff, Michael; Weiss, Manfred
PUB. DATE
December 2001
SOURCE
Intensive Care Medicine;Dec2001, Vol. 27 Issue 12, p1848
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
Objective: To clarify the changes in total leukocyte counts, CD64 neutrophil receptor expression and serum granulocyte colony-stimulating factor (G-CSF) concentrations in critically ill patients without infection and sepsis and in patients with septic shock. Design: Prospective study. Setting: Intensive care unit (ICU) and research laboratory of a university hospital. Patients: Eleven critically ill patients without infections and 22 patients with proven infections in septic shock for the first time and of at least 3 days' duration. Measurements and results: Over a 6month period, a longitudinal analysis of expression of the monomeric Fc receptor type I (CD64, FcγRI) on neutrophils was performed by flow cytometric analysis on a daily basis in all postoperative/post-traumatic patients admitted to the ICU until discharge from the ICU or death. Out of 273 patients, 11 patients without sepsis had organ failure and 22 patients with proven infections had septic shock for the first time and of at least 3 days' duration. Ten out of the 22 patients survived, 12 died. CD64 expression was greater in patients with septic shock than in patients without sepsis. Moreover, CD64 expression was only initially and transiently elevated in most survivors (9/10) and non-survivors (8/12) of septic shock. In survivors, G-CSF serum concentrations were markedly decreased in the 2nd week. Conclusions: Decreased neutrophil CD64 expression in an acutely ill population with septic shock may reflect the development of a non-responsive state as well as the early downregulation of neutrophil activation prior to the resolution of an ongoing infection.
ACCESSION #
15729518

 

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