Nosocomial infections after severe trauma are associated with lower apolipoproteins B and AII

Abstract

BACKGROUND Infection following severe trauma is a significant cause of morbidity and mortality days to weeks after the initial injury. Apolipoproteins play important roles in host defense and circulating concentrations are altered by the acute inflammatory response. The purpose of this study was to determine if patients who acquire infection following severe trauma have significantly lower apolipoprotein levels than trauma patients who do not become infected. METHODS We conducted a case-control study on a prospectively identified cohort of adult patients admitted to our intensive care unit after severe trauma (Injury Severity Score ≥ 16). We compared plasma apolipoprotein levels between patients who acquired an infection within 30 days after trauma (cases) and those that remained infection free (controls). RESULTS Of 40 patients experiencing severe trauma, we identified 22 cases that developed an infection within 30 days after injury. Cases had significantly lower post-trauma plasma levels of apolipoprotein-B (p=0.02) and apolipoprotein-AII (p=0.02) compared to controls. Consistent with previous studies, cases also received greater volumes of crystalloid infusions (p<0.01) and blood transfusions (p<0.01). Cases also had a more profound inflammatory response as measured by Interleukin-6 levels (p=0.02). CONCLUSIONS Infection after severe trauma is associated with decreased circulating apolipoproteins as compared to uninfected controls. Profoundly decreased plasma apolipoproteins B and AII could potentially contribute to the impaired immunity after severe trauma. Apolipoproteins are potential targets for identifying those patients at risk of infection after trauma and for interventions aimed at preventing nosocomial infections.

Serum Lipoproteins Are Critical for Pulmonary Innate Defense against Staphylococcus aureus Quorum Sensing

“…Both models have an approximately 50% reduction in apoB measured in the serum (Fig. 1A,B), consistent with those of trauma patients at risk of infection (9). Using a sub-lethal challenge model (17), we intranasally infected mice with a reporter strain of the agr’ clinical isolate LAC, which expresses YFP under the control of the agr ::P3 promoter (36).…”

“…This illustrates the limited consideration given to the potential health consequences of the other dyslipidemia, severe hypolipidemia and lipoprotein deficiency, often experienced post-trauma and by other critically ill patients (7-9). Since hypolipidemia has been clinically associated with bacterial pneumonia (10-12), we sought to determine the impact of extremely low circulating lipoprotein levels on host innate defense in the lung.…”

“…Interestingly, hyperlipidemia results in impaired intrapulmonary host immunity (6), suggesting that maintenance of normal circulating cholesterol and lipoprotein levels is crucial for optimal host innate defense in the lung. Although severe hypolipidemia, which often accompanies the acute phase response (APR) following surgery or trauma (reviewed in (7-9)), has been associated with bacterial pneumonia (10-12), a critical gap in knowledge remains regarding the impact of extremely low serum lipoprotein levels on host innate defense in the lung.…”

Plasma Lipoproteins as Crucial Components of Host Defence Against Infections

“…Likewise, in the Shipibo people, another indigenous group in the Amazon, the density of parasitic infection correlates inversely to the HDL levels [33]. Further, reduced levels of apolipoproteins in hospital-based studies have been reported to be associated with increased susceptibility to nosocomial infections following severe trauma [34]. However, generalizations are difficult and exceptions to these trends have also been reported [28], and the mechanism involved is not clear.…”

An FcγRIIa polymorphism with decreased C-reactive protein binding is associated with sepsis and decreased monocyte HLA-DR expression in trauma patients

“…Severe sepsis was defined as documented infection with acute organ dysfunction. A subset of this study's patient population was previously characterized (10,21,22). The subjects characterized in this study are part of an ongoing effort to better understand the changes in immune function after severe trauma.…”