A surprising finding in the present study was that there was no increase in the markers of permeability or apoptosis in the B6 mice exposed to mechanical ventilation and LPS, as compared to the lpr mice; instead, the injury response was limited to neutrophilic inflammation and cytokine release. One explanation is that neutrophil recruitment precedes the development of tissue injury in our model, in which the mice were studied relatively early, four hours after the onset of ventilation. Less clear is the finding that the lpr mice actually had increased caspase-3 activity and TUNEL (See figure on previous page.) Figure 8 Anti-KC autoantibody:KC complex deposition in the lungs. FcγRIII (green) and KC (red) in tissue sections from B6 (A) and lpr (B) mice treated with intratracheal E. coli LPS, 15 ng/kg, and exposed to 4 hours of mechanical ventilation (MV) at Tv = 10 cc/kg, FiO2 = 0.21, PEEP = 3. FcγRIII is shown in green, KC is shown in red, and Gr1 (staining leukocytes) is shown in pink. Nuclei are shown in blue. There is an increase signal for both KC and FcγRIII in the B6 mice as compared with the lpr mice. Note the colocalization of KC and FcγRIII. Figure 9 The detection of anti-KC:KC immune complex is specific. Mouse PMN were purified and incubated with either anti-KC-KC immune complexes (first two columns) or with KC alone (third column). Note that the Peprotech antibody, detected only anti-KC-KC immune complexes, whereas the R&D antibody detected only KC. The FcγRIII was labeled green and KC was labeled red.