Serum Concentrations of Lipopolysaccharide-Binding Protein as a Biochemical Marker to Differentiate Microbial Etiology in Patients with Community-Acquired Pneumonia

Abstract

Community-acquired pneumonia (CAP) is a major cause of morbidity and mortality. However, identification of the infecting organism is achievable in only 40–50% of cases, and results are not usually available when the diagnosis of pneumonia is first established (1)(2). Therefore, initial therapy is typically empirical, usually aimed at the standard bacteria, most commonly Streptococcus pneumoniae , and “atypical” pathogens (e.g., Mycoplasma pneumoniae , Legionella species, Chlamydophilia species, and Coxiella burnetii ) that have long been considered the most frequent causes of CAP. Given their effectiveness against S. pneumoniae as well as atypical organisms, macrolide antibiotics have been widely used as initial monotherapy in many cases of CAP. The selection of empirical therapy has become complicated by the emergence of drug-resistant S. pneumoniae , including a growing number of strains resistant to macrolides (1)(2)(3). In light of these uncertainties, clinicians may be inclined to prescribe broad-spectrum antimicrobial coverage for many patients with CAP, a practice that could lead to increasing bacterial resistance over the next few years (3). A patient-specific therapy for CAP that relies on antibiotics with a focused spectrum of activity could improve the care of the individual patient and prevent antibiotic abuse, reducing the risk of microorganisms becoming drug resistant. Therefore, the development of biomarkers to help clinicians predict the microbial etiology of CAP could be useful for selecting patient populations in which this strategy may be appropriate and effective. In fact, a therapeutic strategy based on the concentration of procalcitonin (PCT), a marker of bacterial infection, has recently demonstrated usefulness in reducing antibiotic overuse in lower respiratory tract infections (4). Lipopolysaccharide-binding protein (LBP) is the principal plasma protein responsible for transporting endotoxin molecules to immune effector cells bearing CD14 on their surface (5). High serum LBP concentrations have been found …