Community-acquired pneumonia (CAP) is distinguished from hospital-acquired pneumonia (HAP) according to the time of acquisition of pneumonia and the pathogens involved. Th e Gram-positive bacterium, Streptococcus pneumoniae, is the single most frequent pathogen causing CAP, responsible for up to 60% of cases; Klebsiella pneumoniae, Haemophilus infl uenzae, Staphylococcus aureus, and viruses are isolated in about 10% of cases each and Mycobacterium tuberculosis is more prevalent in developing countries. Knowledge of the expression and role of RAGE in host defense during pneumonia is limited. Morbini et al. observed increased RAGE expression in patients with interstitial and postobstructive pneumonia [32] ; this report left unanswered whether patients with bacterial pneumonia were included in the analysis. Notably, two other studies showed that constitutively present RAGE was not upregulated during pulmonary infl ammation associated with ALI or acute respiratory distress syndrome (ARDS): First, rats with ALI induced by intratracheally administered LPS displayed no change in the distribution of RAGEexpressing cells [29] ; and second, patients with ARDS did not have increased pulmonary expression of RAGE [26] . sRAGE has been suggested to be a lung injury marker based on studies in patients with ALI and on experimental studies in rats [29] . sRAGE was increased in pulmonary edema fl uid and serum from patients with either ALI or ARDS and with hydrostatic pulmonary edema, and in BAL fl uid from rats with either LPS-or hydro chloric acid-induced ALI [29] .