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(Chest. 1999;116:35S-36S.)
© 1999 American College of Chest Physicians

HTI56, An Integral Apical Membrane Protein of the Human Alveolar Type I Cell, Is a Biochemical Marker of Acute Lung Injury*

V. Newman; R. Gonzalez; M. Matthay, MD, FCCP and L. Dobbs, MD, FCCP

* From the Cardiovascular Research Institute, Departments of Pediatrics and Medicine, University of California, San Francisco, CA.

Correspondence to: Dr. V. Newman, University of California San Francisco, Cardiovascular Research Institute, San Francisco, CA 94143-0130.

Although injury to the alveolar epithelial barrier is thought to be of central importance in the pathogenesis of acute lung injury, at the present time (to our knowledge), there are no established biochemical markers for alveolar epithelial injury in human disease. We hypothesized that cell-specific alveolar epithelial apical plasma membrane proteins might be useful biochemical markers for lung injury. This hypothesis has been validated in various models of rodent lung injury, in which the airspace liquid content of RT140, a rat type I cell integral membrane protein, correlated directly with the extent of epithelial injury assessed by morphologic criteria (Am J Physiol 1995; 268:L181–186, and 1997; 272:L631–638). We have now extended these studies to human acute lung injury.

We used a monoclonal antibody against HTI56, an apical integral membrane protein specific to human type I cells (Am J Respir Crit Care Med 1995; 151:A169), to develop a sensitive, quantitative enzyme-linked immunosorbent assay for HTI56. Using this assay, we measured HTI56 in both pulmonary edema fluid and plasma obtained from patients with acute lung injury and from control patients with hydrostatic pulmonary edema. HTI56 in pulmonary edema fluid from 14 patients with acute lung injury (edema fluid protein/plasma protein > 0.75) was 4.5X that (p < 0.0001) of 12 patients with hydrostatic pulmonary edema (clinical history compatible with congestive heart failure, edema fluid protein/plasma protein < 0.65). We measured HTI56 in plasma from these two groups and from 11 normal individuals without cardiovascular or pulmonary disease. Plasma HT156 was similar in normal control subjects (n = 11) and in patients with hydrostatic pulmonary edema (n = 11); in contrast, plasma HTI56 in patients with acute lung injury (n = 12) was 1.6X that (p < 0.05) of normal control subjects.

These results support the hypothesis that HTI56 in pulmonary edema fluid and in plasma may be a novel biochemical marker of human alveolar epithelial cell injury. HTI56 may be useful in clinical studies of acute lung injury to quantify the extent and duration of alveolar epithelial injury, to assess the efficacy of therapeutic modalities, and perhaps to predict impending lung injury.





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