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. Author manuscript; available in PMC: 2017 May 9.
Published in final edited form as: Nat Microbiol. 2016 May 9;1(6):16053. doi: 10.1038/nmicrobiol.2016.53

Figure 2. Innate immune host defences are required for the increased frequency of the colistin-resistant subpopulation during infection.

Figure 2

a, Mice pretreated with PBS liposomes (control, grey) or clodronate liposomes (to deplete macrophages, red) were infected with R/S (pre-infection, black). After 8 h, peritoneal lavage fluid was collected and plated to calculate per cent colistin resistance (n = 5). b, Murine bone-marrow-derived macrophages were untreated or pretreated with cytochalasin D, infected with R/S, and per cent colistin resistance was calculated at the indicated time points (n = 6). c–e, R/S was either untreated or treated with the indicated amounts of H2O2 (c), lysozyme (d) or CRAMP (e) for 5 h, and per cent colistin resistance was calculated (n = 3). f, Wild-type (WT, grey) or triple knockout (TKO, red) mice lacking the gp91 subunit of the NADPH oxidase, lysozyme and CRAMP were infected with R/S (pre-infection, black). At 8 h post-infection, peritoneal lavage fluid was collected and plated to calculate per cent colistin resistance (n = 5). Data are compiled from two independent experiments. Error bars represent s.e.m. Mann–Whitney test (**P < 0.01) in a and f; Student’s two-tailed t-test (*P < 0.05) in b.