Abstract
Acute Lung Injury (ALI) is associated with inflammation and increased alveolar permeability. JAM‐A is localized to tight junctions and expressed by neutrophils, suggesting a role in barrier function and regulating neutrophil migration into the alveolus. To determine whether JAM‐A deletion increases susceptibility to ALI, JAM‐A‐deficient (JAM‐A−/−) and wild‐type (JAM‐A+/+) mice were intraperitoneally injected with 1 mg/kg endotoxin (LPS) to induce ALI. We found that JAM‐A−/− mice displayed elevated levels of alveolar permeability and inflammatory response to LPS‐induced ALI as compared to JAM‐A+/+mice. Both groups displayed the greatest level of inflammation at 24 h, however, lung tissues from JAM‐A−/− mice showed significantly higher vascular congestion and neutrophil infiltrate into the airspace at every time interval examined after LPS treatment when compared to JAM‐A+/+ mice. This suggests that JAM‐A plays an important regulatory role in modulating alveolar barrier function and neutrophil transmigration into the lung. It remains to be determined whether the effect of JAM‐A deficiency is primarily due to an effect on pulmonary endothelium, alveolar epithelium, neutrophils or whether all three cell types are impaired in JAM‐A−/− mice. Supported by: NIH‐HL83120 (MK), NIH‐HL72724 (CAP) and NIH‐ HL84683 (MR).
Published Version
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