Figure 5.
Inactivated H5N1 Avian Influenza Virus Can Induce OxPLs and ALI in Mice
(A) Changes in lung elastance in WT mice following intratracheal administration of vehicle (n = 3), inactivated H1N1 (n = 6), or inactivated H5N1 (n = 8) viruses. ∗p < 0.05 for the whole time course.
(B) Lung edema formation 5 hr after vehicle, inactivated H1N1, or inactivated H5N1 treatment. ∗∗p < 0.01.
(C) Immunohistochemistry for influenza A nucleoprotein in lung of WT mice challenged with vehicle, inactivated H1N1, or inactivated H5N1 viruses. Influenza A protein-positive cells were present in the lower respiratory tract including alveolar macrophage (arrowhead) and pneumocytes (arrows). Original magnifications × 400.
(D) ROS expression in alveolar macrophages from WT mice treated with control vehicle (blue), inactivated H1N1 virus (white, upper panel), or inactivated H5N1 virus (white, lower panel).
(E) TLR4 expression in alveolar macrophages from WT mice treated with vehicle (blue), inactivated H1N1 virus (white), or inactivated H5N1 virus (white). Representative histograms are shown for five separate experiments. Data in (D) and (E) are at 1 hr after viral challenge.
(F) Immunohistochemistry for influenza A nucleoprotein and EO6-detectable OxPLs in lung of WT mice infected with live H5N1 avian influenza virus. H5N1-infected mice contain large numbers of influenza A protein-positive cells (brown) in the lower respiratory tract (left panels, arrowheads). OxPLs were localized to inflammatory cells (arrowheads) as well as inflammatory exudates (arrow). Lungs were analyzed 4 days after infection. Original magnifications × 100 (upper panels) and × 200 (lower panels). Data are mean values ± SEM.