Th is putative functional role of RAGE in healthy lungs may be the explanation for the fi nding that the inhibition of RAGE signaling attenuates pathological sterile infl ammatory responses in diverse non-pulmonary experi mental studies [9] [10] [11] [12] , whereas in pulmonary non-infectious pathological infl ammatory conditions, somewhat confl ict ing results emerge. Lung injury induced by either bleomycin or hyperoxia is diminished in RAGE -/mice [37, 38] , suggesting a deteriorating attribution of RAGE. In contrast, Englert et al. showed that RAGE -/mice developed more severe lung fi brosis after asbestos adminis tration as measured by histological scoring and total lung hydroxyproline quantifi cation [31] . Of note, in all these studies, the mice were much younger at the time of sacrifi ce than the aged (19-24 month-old) RAGE -/mice that developed pulmonary fi brosis spontaneously in the experiment by Englert et al. [31] . Interestingly, lung homogenates and bronchoalveolar lavage (BAL) fl uid from patients suff ering from idiopathic pulmonary fi brosis reveal reduced membrane bound (and soluble) RAGE protein levels compared to healthy donor samples [31, 34] . 