Human Monocytes - CD14, CD16 - Ziegler-Heitbrock


C-C Chemokine Receptor Type 2 Expression on Monocytes Before Sepsis Onset Is Higher Than That of Postsepsis in Septic Burned Patients: A New Predictor for Sepsis in Burned Injury.


OBJECTIVE: The present study aims to investigate the alterations in monocytes (Mo) and dendritic cells (DCs) in septic burned patients with a special focus on C-C chemokine receptor type 2 (CCR2) expressions on classical Mo. BACKGROUND: The phenotypes of Mo and DCs, particularly CCR2 expression on Mo, are not fully explored in severely burned patients with sepsis. METHODS: The prospective cohort study was conducted in Ross Tilley Burn Centre and Sunnybrook Research Institute (Toronto, Canada). We enrolled 8 healthy patients and 89 burned patients with various burned sizes, of those burned patients, 12 were with sepsis. Blood was collected upon admission to the hospital and throughout their course in hospital. The expression of human leukocyte antigen-DR was determined on all DCs and Mo, along with CCR2 on CD14/CD16 Mo. RESULTS: We found a profound decrease in human leukocyte antigen-DR on Mo and DCs in burned patients with sepsis compared with healthy controls and nonseptic burned patients. In addition, septic burned patients presented an increased CCR2 expression on classical Mo (CD14/CD16), which was paralleled by greater chemokine (C-C motif) ligand 2 concentrations in the plasma when compared with controls and nonseptic burned patients. Furthermore, burned patients with sepsis had a more profound expansion of CD14/CD16 Mo when compared with nonseptic burned patients. CONCLUSION: Our results demonstrate that burned patients with sepsis have more profound impairment of monocytes and dendritic cells than burned patients without sepsis. With CCR2 level on Mo before sepsis onset being higher than postsepsis, CCR2 expression could be a new predictor of sepsis onset in severe burn injury.

Authors: Xiu F, Stanojcic M, Wang V, Qi P, Jeschke MG.
Journal: Ann Surg. 2016 Aug;264(2):392-8.
Year: 2016
PubMed: Find in PubMed