Recent evidence in knockout mice suggests that G-CSF may play a previously unreported, relevant pathogenic role in COPD (Tsantikos et al., 2018); CHF6001 marked inhibition of G-CSF production may therefore contribute to the overall control of the inflammatory response elicited by bacterial lipopolysaccharides in our model as well as during infection-driven exacerbations in COPD subjects. Here, CSF3 is linked to infection.