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The dual fate of CMo as suggested by our study is supported by previous fate mapping studies demonstrating that Ly6C hi CMo differentiate into IM and that AM recruited into the alveolar space following influenza infection originate from CCR2-dependent bone marrow-derived monocytes ( AM of monocytic origin have been recently shown to differ in their molecular response and function from ResAM during acute influenza infection and in models of pulmonary fibrosis ( Wfdc17 / 21 ( Among the various pro-inflammatory mediators strongly expressed by MoAM several are linked to COPD including CCL2 and CCL7 , which have been shown to be increased in induced sputum of COPD patients ( Ccl2/Ccl7 by murine MoAM, we hypothesize that small sputum macrophages reflect their human orthologs and correspond to the human CCL2 + mono-like macrophages that were increased in BALF of the emphysematous COPD patients

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