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. 2013 Apr;48(4):477–488. doi: 10.1165/rcmb.2012-0242OC

Figure 6.

Figure 6.

The knockdown of NOX2 expression attenuates P. aeruginosa–induced lung inflammation, but with no loss of endothelial permeability. (A–E) gp91phox−/− knockout mice were exposed to P. aeruginosa for 24 hours. BAL was collected, and its cell count (D), protein content (E), and IL-6 (A), TNF-α(Β), and H2O2 (C) concentrations were measured as described in Materials and Methods. *P < 0.01, compared with wild-type (WT) control samples. **P < 0.01, compared with gp91phox−/− control samples (n = 5). #P < 0.01, compared with wild-type control samples. ##P < 0.05, compared with the wild-type PA treatment group (n = 5). (F) C57BL/6J and gp91phox−/− were exposed to P. aeruginosa for 24 hours C57BL/6J had significant evidence of lung injury and inflammation, whereas gp91phox−/− mice exhibited significantly fewer instances of alveolar damage and inflammatory response. Images are representative of four mice for each group. Original magnification, ×200.