Bronchoalveolar interleukin-1β

Objective: To assess the relationship between concentrations of bronchoalveolar cytokines and bacterial burden (quantitative bacterial count) in intubated patients with a presumptive diagnosis of community-acquired pneumonia. Design: A cross-sectional and clinical investigation. Setting: Medical/surgical and respiratory intensive care unit of a tertiary 1,200-bed medical center. Patients: According to the time course of community-acquired pneumonia at the time of study with bronchoalveolar lavage, 69 mechanically ventilated patients were divided into three subgroups: primary (n = 11), referral (n = 23), and treated (n = 35) community-acquired pneumonia. Interventions: Bronchoalveolar lavage was performed in the most abnormal area on chest radiograph by fiberoptic bronchoscope. Bronchoalveolar lavage fluid was processed for quantitative bacterial culture. The concentrations of bronchoalveolar lavage cytokines (tumor necrosis factor-α, interleukin-1β, interleukin-6, interleukin-8, and interleukin-10) also were measured. Measurements and Main Results: Thirty-two patients had a positive bacterial culture (bronchoalveolar lavage ≥103 colony-forming units/mL). Pseudomonas aeruginosa, Acinetobacter baumannii, Staphylococcus aureus, and Klebsiella pneumoniae made up 76% of pathogens recovered at high concentrations. The concentrations of bronchoalveolar lavage interleukin-1β were 199.1 ± 32.1 and 54.9 ± 13.0 pg/mL (mean ± SE) in the patients with positive and negative bacterial culture, respectively (p < .001). Bronchoalveolar lavage interleukin-1β was significantly higher in the patients with a high bacterial burden (p < .001), with mixed bacterial infection (p < .001), and with P. aeruginosa pneumonia (p < .001), compared with values in patients without these features. The relationship between bacterial load and concentrations of bronchoalveolar lavage interleukin-1β was very strong in the patients with primary and referral community-acquired pneumonia but was borderline in treated community-acquired pneumonia. Conclusions: The common pathogens were similar to the core pathogens of hospital-acquired pneumonia, probably due to antibiotic effects, delayed sampling, and superimposed nosocomial infection. Since the concentration of bronchoalveolar lavage interleukin-1β was correlated with bacterial burden in the alveoli, it may be a marker for progressive and ongoing inflammation in patients who have not responded to pneumonia therapy and who have persistence of bacteria in the lung.