Guilherme Eckert Peterson

Transforming growth factor beta1 (TGF-ß1) levels in a rat model of induced pleural empyema

PURPOSE To evaluate the concentration of transforming growth factor beta 1 (TGFB1) levels in a rat pleural effusion obtained by inoculation of intrapleural bacteria or turpentine through thoracentesis. METHODS Thirty-Nine Wistar rats were divided into three groups: Staphylococcus aureus (SA, n = 17); Streptococcus pneumoniae (SP, n = 12); and turpentine (control, n = 10). Pleural fluid was collected through ultrasound-guided thoracentesis 12 h, 24 h, and 36 h after instillation of bacteria or turpentine. Levels of TGFB1 were measured in pleural fluid. RESULTS At 12 h, mean TGFB1concentrations were 5.3450 pg/mL in the SA group, 5.3449 pg/mL in the SP group, and 5.3450 pg/mL in controls. At 24 h, they were 4.6700 pg/mL in the SA group, 4.6700 pg/mL in the SP group, and 4.6700 pg/mL in controls. At 36 h, they were 4.6699 pg/mL in the SA group and in control. No difference was observed among the groups in mean TGFB1concentration (p = 0.12); however, a significant intragroup reduction in mean TGFB1 was observed between 12 and 24 h (p < 0.01). CONCLUSION The transforming growth factor beta 1 concentrations were not useful as a diagnostic tool or an early marker of infected pleural effusion.

Accuracy of complement activation product levels to detect infected pleural effusion in rats

Background: Pleural empyema is a well‐known complication of pneumonia. If treatment is delayed, empyema may increase morbidity and mortality in affected patients. Therefore, the identification of empyema biomarkers in parapneumonic pleural effusion is desirable. Previous research has suggested complement activation products as candidate empyema markers. Objective: To compare the levels of complement activation products C3a, C5a, and C5b9 in pleural effusion induced by Staphylococcus aureus (SA), Streptococcus pneumoniae (SP), or turpentine (control). Methods: Thirty‐nine male Wistar rats (mean weight 414 g; 290–546 g) were allocated as follows: 17 animals in the SA group, 12 in the SP group, and 10 in the control group. Bacteria or turpentine were injected into the pleural space. After 12 hr, intrapleural fluid was collected using ultrasound‐guided thoracentesis. Levels of complement activation products were determined using ELISA kits. Results: Two SA and one SP animals died before 12 hr. Mean levels were as follows: C3a: 1066.82 µg/ml (937.29–1196.35 µg/ml) in SA, 1188.28 µg/ml (1095.65–1280.92 µg/ml) in SP, and 679.13 µg/ml (601.29–756.98 µg/ml) in controls (P < 0.001); C5a: 55.727 ng/ml (41.22–70.23 ng/ml) in SA, 520.107 ng/ml (278.92–761.3 ng/ml) in SP, and 5.268 ng/ml (1.68–8.85 ng/ml) in controls (P < 0.001); C5b9: 15.02 ng/ml (13.1–16.94 ng/ml) in SA, 16.63 ng/ml (14.37–18.9 ng/ml) in SP, and 14.05 ng/ml (9.8–18.29 ng/ml) in controls (P = 0.692). ROC analysis revealed an area under the curve of 0.987 (95% CI: 0.953–1) for C3a; 1 (1–1) for C5a; and 0.757 for C5b9 (0.523–0.990). Conclusions: In the present rat model, complement activation fragments C3a and C5a accurately detected infected pleural effusion. Pediatr Pulmonol. 2017;52:757–762.