Figure 5
Figure 5. Modulation of NET formation by DNAse1 or neutrophil elastase influences neutrophil recruitment, vascular permeability, and severity of VILI. WT mice with or without DNAse1 pretreatment and DNAse1−/−/Trap1m/m (DNAse1−/−) mice and neutrophil elastase–deficient (NE−/−) mice were ventilated with sham or VILI settings. (A) The paO2/FiO2 ratio, (B) neutrophil recruitment into the alveoli, and (C) protein concentration in the BAL were analyzed after 2 hours (n = 4). (D) The formation of circulating platelet-neutrophil aggregates was measured by flow cytometry 30 minutes after induction of sham or VILI ventilation (n = 4). (E) Circulating NET structures were quantified by MPO-DNA-ELISA (n = 4). *P < .05.

Modulation of NET formation by DNAse1 or neutrophil elastase influences neutrophil recruitment, vascular permeability, and severity of VILI. WT mice with or without DNAse1 pretreatment and DNAse1−/−/Trap1m/m (DNAse1−/−) mice and neutrophil elastase–deficient (NE−/−) mice were ventilated with sham or VILI settings. (A) The paO2/FiO2 ratio, (B) neutrophil recruitment into the alveoli, and (C) protein concentration in the BAL were analyzed after 2 hours (n = 4). (D) The formation of circulating platelet-neutrophil aggregates was measured by flow cytometry 30 minutes after induction of sham or VILI ventilation (n = 4). (E) Circulating NET structures were quantified by MPO-DNA-ELISA (n = 4). *P < .05.

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