Abstract
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. 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. 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). The transforming growth factor beta 1 concentrations were not useful as a diagnostic tool or an early marker of infected pleural effusion.
Highlights
Complicated parapneumonic pleural effusion (CPPE) remains a challenging problem[1], and current literature on the subject emphasizes the importance of early diagnosis[2,3]
Review Board, thirty nine male Wistar rats, mean weigh 414 g (290 to 546 g), were divided into three different groups: 17 animals were inoculated with 0.1 mL brain-heart infusion containing Staphylococcus aureus at a concentration of 1010 colony forming units (CFU)/mL (SA group); 12 animals were inoculated with 0.05 mL brain-heart infusion containing Streptococcus pneumoniae at a concentration of 1010 CFU/mL (SP group); and 0.2 mL turpentine was administered to 10 control animals (Group C)
There were no deaths in the control group, but one control animal did not develop pleural fluid
Summary
Complicated parapneumonic pleural effusion (CPPE) remains a challenging problem[1], and current literature on the subject emphasizes the importance of early diagnosis[2,3]. Early diagnosis and treatment are believed to be crucial to reduce CPPE morbidity and mortality in both adult and pediatric populations. Cytokines have been identified as promising early markers of parapneumonic effusion and empyema. Due to the difficulty in designing prospective population-based studies on CPPE and controlled studies for diagnostic evaluation and testing of therapeutic strategies, experimental animal models have been playing an important role in the search for biological markers of pleural infection and empyema. Most experimental models of pleural effusion or empyema described in the literature have employed pigs[6,7,8] or rabbits[9,10]. A new rat model of empyema has been successfully developed[11,12], with greater reproducibility and lower cost and housing infrastructure than those of rabbits or pigs
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