Published in:
Open Access
01-12-2011 | Research article
TREM-1 expression on neutrophils and monocytes of septic patients: relation to the underlying infection and the implicated pathogen
Authors:
Thekla Poukoulidou, Aikaterini Spyridaki, Ira Mihailidou, Petros Kopterides, Aikaterini Pistiki, Zoi Alexiou, Michael Chrisofos, Ioanna Dimopoulou, Panagiotis Drimoussis, Evangelos J Giamarellos-Bourboulis, Ioannis Koutelidakis, Androniki Marioli, Anna Mega, Stylianos E Orfanos, Maria Theodorakopoulou, Christos Tsironis, Nina Maggina, Vlassios Polychronopoulos, Iraklis Tsangaris, the Hellenic Sepsis Study Group
Published in:
BMC Infectious Diseases
|
Issue 1/2011
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Abstract
Background
Current knowledge on the exact ligand causing expression of TREM-1 on neutrophils and monocytes is limited. The present study aimed at the role of underlying infection and of the causative pathogen in the expression of TREM-1 in sepsis.
Methods
Peripheral venous blood was sampled from 125 patients with sepsis and 88 with severe sepsis/septic shock. The causative pathogen was isolated in 91 patients. Patients were suffering from acute pyelonephritis, community-acquired pneumonia (CAP), intra-abdominal infections (IAIs), primary bacteremia and ventilator-associated pneumonia or hospital-acquired pneumonia (VAP/HAP). Blood monocytes and neutrophils were isolated. Flow cytometry was used to estimate the TREM-1 expression from septic patients.
Results
Within patients bearing intrabdominal infections, expression of TREM-1 was significantly lower on neutrophils and on monocytes at severe sepsis/shock than at sepsis. That was also the case for severe sepsis/shock developed in the field of VAP/HAP. Among patients who suffered infections by Gram-negative community-acquired pathogens or among patients who suffered polymicrobial infections, expression of TREM-1 on monocytes was significantly lower at the stage of severe sepsis/shock than at the stage of sepsis.
Conclusions
Decrease of the expression of TREM-1 on the membrane of monocytes and neutrophils upon transition from sepsis to severe sepsis/septic shock depends on the underlying type of infection and the causative pathogen.