In particular, as the only cell population with significantly lower podoplanin expression solely in Pdpnfl/flVAV1cre+ mice following LPS (Fig. 5C), loss of podoplanin from BAL CD11b+CD11c+F4/80+ alveolar inflammatory macrophages may play a key role in limiting endotoxemia-induced inflammation in the lung. This evidence concerns the gene ITGAM and serum lipopolysaccharide activity.