We and others have postulated that the Fas/FasL system leads to lung injury by inducing apoptosis of pneumocytes, resulting in disruption of the alveolar-epithelial barrier and non-cardiogenic pulmonary edema. However, in the present study the BAL concentration of total protein and of the serum protein α-macroglobulin were similar in the lpr and B6 mice, despite the difference in PMN numbers ( Figure 2 ). The lack of difference may be due to a low level of injury, as supported by the lack of overall change in the MV + LPS group as compared with the SB group; indeed the model was designed so that the ventilatory pattern and the LPS dose would cause minimal or no injury by themselves, so as to determine the very first components of the injury response. The data suggest that neutrophil changes precede permeability changes in ventilated mice exposed to LPS, and that the role of the Fas/FasL system on neutrophil recruitment precedes its disruptive effect on the alveolar-capillary barrier.