摘要：SummaryMoraxella catarrhalisand nontypeableHaemophilus influenzae(NTHi) are pathogenic bacteria frequently associated with exacerbation of chronic obstructive pulmonary disease (COPD), whose hallmark is inflammatory oxidative stress. Neutrophils produce reactive oxygen species (ROS) which can boost antimicrobial response by promoting neutrophil extracellular traps (NET) and autophagy. Here, we showed thatM. catarrhalisinduces less ROS and NET production in differentiated HL-60 cells compared to NTHi. It is also able to actively interfere with these responses in chemically activated cells in a phagocytosis and opsonin-independent and contact-dependent manner, possibly by engaging host immunosuppressive receptors.M. catarrhalissubverts the autophagic pathway of the phagocytic cells and survives intracellularly. It also promotes the survival of NTHi which is otherwise susceptible to the host antimicrobial arsenal. In-depth understanding of the immune evasion strategies exploited by these two human pathogens could suggest medical interventions to tackle COPD and potentially other diseases in which they co-exist.Graphical abstractDisplay OmittedHighlights•Mcat induces ROS and NET production to a lesser extent than NTHi in dHL-60 cells•Mcat interferes with ROS-related responses in chemically-activated cells•Mcat subverts the autophagic pathway surviving intracellularly while NTHi does not•Intracellular survival of NTHi is enhanced by the co-infecting bacterium McatMicrobiology, molecular microbiology, immune response, and microbial physiology
