Complete reversal of acid-induced acute lung injury by blocking of platelet-neutrophil aggregation
J. Clin. Invest. Alexander Zarbock, et al. 116:3211 doi:10.1172/JCI29499 [Go to this article.]

Figure 1
Platelets control PMN recruitment into the lung in acid-induced ALI. (A–C) Platelet depletion (by 40%) prior to acid application by busulfan (n = 4–10 mice per group) significantly improved gas exchange (A), reduced intravascular and interstitial PMN accumulation (data not shown), diminished PMNs in the BAL fluid (B), and partially prevented increased vascular permeability (C). Platelet depletion (85%) caused by a polyclonal Ab diminished PMN recruitment into the alveolar space (B) and permeability (C). (D–G) Photomicrographs of lung tissue. H&E-stained paraffin sections from control mice (D) and mice 2 hours after acid administration (E). Acid application induced increased permeability with an influx of protein-rich fluid and cells (E, arrow) into the alveolar space, swelling of the interstitium, and cell accumulation in the interstitial space (E). Glycol pretreatment (F) prior to initiation of ALI induced the same histological changes seen in untreated mice after acid application whereas the pretreatment with busulfan led to reduced morphological changes (G). Original magnification, ×65. Gly, glycol; Bu, busulfan; pre, preimmune serum; Ab, polyclonal anti-platelet Abs. ^#P < 0.05. Scale bars, 50.0 mm.