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Dear Editor, Alveolar macrophages (AM) express a unique repertoire of matrix metalloproteinases (MMPs) that have downstream effects on inflammatory mediators involved in acute respiratory distress syndrome (ARDS) pathogenesis. MMP28 is the newest member of the MMP family and has been shown to be upregulated in inflammatory conditions such as idiopathic pulmonary fibrosis [1]. In animal models of lung infection, MMP28 plays a key role in macrophage chemotaxis [2] and in modulating macrophage polarity [3]. AM polarization plays a central role in orchestrating alveolar inflammation and repair in ARDS, and we have previously shown that AM transcriptional programs are associated with ARDS clinical outcomes such as ventilator-free days (VFDs) [4]. Therefore, our primary hypothesis was that AM MMP28 gene expression is associated with VFDs in subjects with ARDS. Secondarily, we hypothesized that AM MMP28 gene expression and alveolar MMP28 concentrations are associated with PaO2/FiO2 ratio (P/F ratio), percentage alveolar neutrophils (% PMNs), and total protein levels. We analyzed bronchoalveolar lavage fluid (BALF) from subjects previously enrolled in a phase-II trial [5] of omega-3 fatty acids for the treatment of ARDS (n = 76) (Table 1). In a subset of these patients (n = 25), AMs were purified from BALF by negative selection as previously described [4]. Samples were obtained from subjects within 48 h of ARDS onset and prior to them receiving

Alveolar MMP28 is associated with clinical outcomes and measures of lung injury in acute respiratory distress syndrome