Introduction and Objectives:
During bacterial stress, neutrophils express activation markers such as CD64. It has been demonstrated in mechanically ventilated patients with ARDS related to SARS-CoV-2 that the observation of circulating CD16low immature granulocytes (IGs) expressing the CD64 marker was related to bacterial co-infection. Here, we aim to determine in patients without pulmonary infection whether the emergence of this sub-population over time is associated with the development of ventilator-associated pneumonia (VAP).
Materials and Methods:
Immunocompetent patients who were ventilated for at least 24 hours for a traumatic brain injury (TBI) or a stroke were included in this prospective single-center study. During the first week of the hospital stay, the expression of several markers on granulocytes and plasma concentration of pro-inflammatory cytokines were assessed daily. Two independent physicians blinded from the flow cytometry results adjudicated all patients and determined the date of onset of VAP or ventilator-associated tracheobronchitis (VAT) when applicable.
Results:
Forty patients have been included (13 TBI, 27 strokes; median age 54 ± 15 years). After adjudication, 5 VAP and 14 VAT were confirmed (47%). We found that CD16low/CD64+ IGs level is similar between groups of patients over time (patients without pulmonary infection median = 0.27% [25-75 percentiles: 0.12-1.109]; patients with VAT median = 0.35% [0.15-1.48] and patients with VAP median = 0.38% [0.13-3.55]). However, a peak was observed within one day of VAP clinical diagnosis with values above the 75 percentile for three out of five patients (36.71%, 57.12%, 52.94%) and an increasing level of IL-6 (> 1000 pg/mL) and G-CSF (> 160 pg/mL).
Conclusion:
These preliminary results seem to associate the development of VAP with increased circulating CD16low/CD64+ IGs. The recruitment of this sub-population is presumably related to the increased level of G-CSF that stimulates neutrophil production and CD64 expression.