Is the measurement of monocytes HLA-DR expression useful in patients with sepsis?

Excerpt

Leukocytes undergo significant reprogramming in patients with sepsis [1]. Compared with monocytes from healthy subjects, monocytes from patients with severe infections lose their capacity to mount a pro-inflammatory response after stimulation with bacterial products. Not only do they produce less pro-inflammatory cytokines, they also increase their production of anti-inflammatory mediators and receptor antagonists, such as the monocyte de-activating interleukin (IL)-10 and IL-ra [2]. This gives the plasma a dominant “anti-inflammatory” flavor [3]. It has been proposed that this phenomenon is a compensatory reaction to the initial inflammatory response [4]. We believe that this is an essential adaptive systemic response aimed at concentrating the inflammatory response at the site of infection, in the organs [5]. A decreased surface expression of major histocompatibility class II molecules was also described in circulating monocytes from patients with sepsis, as well as in other critically ill patients. This is associated with an impaired antigen presentation capacity. The association of a decreased HLA-DR expression and a blunted pro-inflammatory cytokine production by monocytes is also known as “immunoparalysis” [6]. The molecular mechanisms of HLA-DR downregulation at the surface of monocytes from critically ill patients are now better understood. HLA-DR production is impaired, and is retained intracellularly [7, 8, 9, 10]. Interestingly, this monocyte phenotype can be reversed by the treatment of septic patients with interferon-γ or granulocyte--monocyte colony-stimulating factor [11, 12, 13]. Unfortunately, these studies were not powered to demonstrate an improvement in survival in patients with severe sepsis, nor did they show a convincing decrease in the rate of secondary infections. …