Background. The triggering receptor expressed in myeloid cells (TREM-1) is a key mediator in the activation of the local inflammatory response during lung infections. We aimed to evaluate the effect of a functionally relevant TREM-1 single nucleotide polymorphism within the exon 2 (A→T) on the development of pneumonia in burn patients. Objective. To determine whether a single nucleotide polymorphism (SNP) within the exon 2 (A→T) in the TREM-1 gene is associated with ventilator-associated pneumonia (VAP) in burn-injured patients. Methods. 540 patients with ≥10% total body surface area (TBSA) burn injuries or inhalation injury were prospectively enrolled. The influence of a polymorphism (A→T) in exon 2 of the TREM-1 gene was evaluated for association with increased risk of pneumonia by logistic regression analysis. Measurements and Main Results. 209 patients met criteria for VAP. Multivariate regression analysis showed that, after adjustment for potential confounders, we found that carriage of the TREM-1 T allele is associated with more than a 3-fold increased risk of VAP (OR 6.3, 95% CI 4–9). Conclusions. A TREM-1 single nucleotide polymorphism within the exon 2 (A→T) is associated with the development of pneumonia in burn patients. 1. Introduction Ventilator-associated pneumonia (VAP) is a common complication in patients receiving mechanical ventilation in the burn intensive care unit (BICU) [1]. VAP results in substantial increase in morbidity and mortality [2–4]. Even though pneumonia is very common in the burn patient, the clinical and demographic factors that might predict who is at risk for developing VAP are nonspecific [5–9]. Additionally, the accuracy of standard clinical and laboratory methods of VAP diagnosis remains under constant scrutiny, and there is increasing debate concerning whether VAP is a preventable disease [10, 11]. The type of insult and clinical presentation of the patient do not predict which individuals will develop VAP and subsequent progression to sepsis, multi-system organ failure, or death [8, 9, 12–14]. There is a wide range of clinical responses to similar types and degrees of insult (i.e., not all patients with the same degree of burn and physiological similarities will go on to develop pneumonia). Similarly, different patients will often respond differently to the same treatment regimen. These differences may well reflect genetic differences amongst individuals [15–19]. Significant associations have been observed between specific SNPs and clinical outcome after burn and trauma [20–26]. The triggering receptor expressed
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