Measurement of functional and morphodynamic neutrophil phenotypes in systemic inflammation and sepsis

Abstract

We read with great interest the review by Leliefeld et al. [1] published in Critical Care on the role of neutrophils in immune paralysis during systemic inflammation (SI). This is of high clinical importance since immune paralysis potentially increases susceptibility to new infections or may cause inability to clear existing infections, leading to detrimental outcome. One mechanism proposed for immune paralysis is the release of neutrophil populations with decreased microbicidal properties [1]. During SI, heterogeneous subsets of neutrophils exist with different priming states and functions [2]. In particular, large numbers of immature neutrophils appear in the circulation with diminished expression of receptors, important for pathogen killing [3]. We recently reviewed the literature on morphodynamic changes in neutrophils during sepsis [4]. Sepsis increases neutrophil circulating numbers (and percentages of immature neutrophils) and their cell size and stiffness, and decreases migration/chemotaxis, compared with nondiseased conditions or mild infection. Septic neutrophils are also prone to produce neutrophil extracellular traps (NETs).