Figure 6

Figure 6

Ramipril and MDIVI-1 treatment alters the respiratory burst response in IAV systemically infected zebrafish at 48 hpi. (A) Respiratory burst response in larvae treated with DMSO, ramipril (0.2 nM), and MDIVI-1 (7 nM) at 48 hpi following systemic injection at 3 dpf with PR8 or HBSS. PR8 infection decreased the response over HBSS in DMSO-treated controls (adjusted p = 0.0008). Both ramipril and MDIVI-1 treatment remedied the reduction in respiratory burst response, as the PR8-infected larvae had the same response as HBSS-injected controls (comparisons were not significant (ns)). The protein kinase C inhibitor bisindolylmaleimide I (BisI) was used as a positive control as it suppresses the respiratory burst response (adj. p < 0.0001 for all comparisons). (B) Respiratory burst response in larvae treated with DMSO, ramipril (0.2 nM), and MDIVI-1 (7 nM) at 48 hpi following systemic injection at 3 dpf with mVenus-PR8 or HBSS. Similar to the PR8-infected larvae, mVenus-PR8 infection decreased the response over HBSS in DMSO-treated controls (adj. p = 0.0040). Ramipril treatment resulted in a higher respiratory burst response with mVenus-PR8 infection than HBSS controls (adj. p = 0.0049). MDIVI-1 treatment remedied the reduction in respiratory burst response as the mVenus-PR8-infected larvae had the same response as HBSS injected controls. The BisI controls were different to the DMSO (adj. p < 0.0001 for both), ramipril (adj. p = 0.0003 for HBSS, and adj. p < 0.0001 for mVenus-PR8), and MDIVI-1 (adj. p = 0.0006 for HBSS, ns for mVenus-PR8) groups. Not significant (ns), p > 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001.