The Role of the Scavenger Receptor B Family Proteins (SR-BI, SR-BII and CD36) in Infection and Sepsis

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Abstract

Using human SR-BI (hSR-BI) and human SR-BII (hSR-BII) transgenic mice, we have found that SR-BI and, to a lesser extent, SR-BII protect against bacterial LPS-induced lung damage: At 20 hours after intratracheal LPS instillation, the extent of pulmonary inflammation and vascular leakage was significantly lower in hSR-BI and hSR-BII transgenic mice compared to wild type mice. Higher bronchoalveolar lavage fluid (BALF) inflammatory cell counts and protein content, as well as lung tissue neutrophil infiltration were found in wild type mice. In addition, there was increased pro-inflammatory cytokine production (2-3 fold) when compared to transgenic mice following IT LPS administration. Markedly lower endotoxin levels detected in broncho-alveolar lavage of transgenic vs. wild type mice along with significantly increased BODIPY-LPS uptake were observed in lungs of hSR-BI and hSR-BII mice 20 hours after the IT LPS injection. These results suggest that hSR-BI and hSR-BII mediated enhanced LPS clearance in the airways could represent the mechanism for their protective role against LPS-induced acute lung injury, a model of bacterial infection lung damage. We have begun to evaluate the role of class B scavenger receptors in the pathogenesis of SARS-CoV-2 and other viruses.