Guillaume Monneret, MD

Author address: 

Universite Lyon, France


Intensive Care Unit (ICU)-acquired immunosuppression represents a major although largely underrecognized healthcare problem worldwide accounting for thousands of deaths every year. It is now agreed that various types of injury (sepsis, burn, trauma, surgery, pancreatitis) deeply perturb immune homeostasis by inducing an initial tremendous systemic inflammatory response (SIRS) which is accompanied by an anti-inflammatory process, acting as a negative feedback. This compensatory inhibitory response secondly becomes deleterious as nearly all immune functions are compromised including lymphocyte, monocyte, dendritic cell alterations. These alterations might be directly responsible for worsening outcome as they may play a major role in the decreased resistance to nosocomial infections in patients who survived initial resuscitation. As evidence, an important part of nosocomial infections observed in ICU patients are due to commensals, which become pathogenic solely in fragile, immunocompromised host. This is especially true for fungal infections. To date, no clinical signs are relevant for the diagnosis of immunosuppression in these patients. This presentation focuses on immune dysfunctions described so far in septic patients and on related biomarkers usable on a routine standardized basis for prediction of adverse outcome and occurrence of secondary nosocomial infections. Such a monitoring could be useful in clinical practice to identify at-risk patients in whom an adapted strategy has to be applied, such as intensive screening of infections, limitation of as much as possible other risk factors (catheters, invasive device), and directed immunostimulation, if necessary. Such an immunostimulating therapeutic strategy might improve patients’ immune response and thus limit the occurrence of secondary infections or accelerate their resolution. While different drugs (IFNg, GM-CSF) have been already assessed in this condition and others appear as good candidates (IL-8, Flt3-L), this approach requires additional clinical trials. This aspect will be evoked in the presentation as well.

abstract No: 


Full conference title: 

4th Advances Against Aspergillosis
    • AAA 4th (2010)