Prolonged in vitro anti-bacterial, anti-inflammatory, and surfactant-promoting effects of volatile anesthetics

Volatile anesthetics are gaining recognition for their benefits in long-term sedation of mechanically ventilated patients with bacterial pneumonia and acute respiratory distress syndrome. In addition to their sedative role, they also exhibit anti-bacterial and anti-inflammatory properties, though the mechanisms behind these effects remain only partially understood. In vitro studies examining the prolonged impact of volatile anesthetics on bacterial growth, inflammatory cytokine response, and surfactant proteins - key to maintaining lung homeostasis - are still lacking.

Using an anaerobic chamber setup, we evaluated the effects of the most commonly used volatile anesthetics, Sevoflurane and Desflurane, at clinically relevant concentrations on the growth of Pseudomonas aeruginosa, Escherichia coli, and Staphylococcus aureus. Bacterial growth was monitored over 24 h, assessing OD₆₀₀, CFU/ml, and growth rate during the log phase. In the same setup, but with aerobic conditions, we investigated the immunomodulatory properties of both anesthetics on human A549 cells, either with or without bacterial lipopolysaccharide (LPS, 1 µg/ml) stimulation. Over 48 h, we analyzed pro-inflammatory chemokine release using ELISA and assessed surfactant protein expression with Western blot analysis.

Sevoflurane and Desflurane significantly reduced Pseudomonas aeruginosa growth as expressed consistently in OD₆₀₀ and CFU/ml starting after 12 h. Both volatile anesthetics also significantly reduced Staphylococcus aureus OD₆₀₀ starting after 21 h. Sevoflurane (p < 0.01) and Desflurane (p < 0.001) counteracted LPS-induced interleukin-8 release by A549 cells after 48 h and significantly ( p < 0.01 and p < 0.05) enhanced the expression of the propeptide of surfactant protein C after 24 h.

Prolonged anti-bacterial and anti-inflammatory effects of Sevoflurane and Desflurane include both the reduction of Pseudomonas aeruginosa and Staphylococcus aureus growth as well as the inhibition of LPS-induced chemokine release by A549 epithelial cells paralleled by an increase of surfactant protein expression. These effects highlight the potential of volatile anesthetics beyond sedation in supporting lung function in ventilated patients with respiratory failure.