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. 2008 Apr 17;133(2):235–249. doi: 10.1016/j.cell.2008.02.043

Figure 7.

Figure 7

The Oxidative Stress Machinery Controls the Severity of ALI in Response to Inactivated H5N1 Avian Influenza Viruses

(A) ROS expression in control PBMCs and PBMCs from the same donor treated with inactivated H1N1 or inactivated H5N1 viruses. Data are from CD14+ gated PBMCs. Representative histograms are shown for six separate donors.

(B) TLR4 expression in control human PBMCs and H5N1- or H1N1-treated PBMCs. Data are from CD14+ gated PBMCs. Representative histograms are shown for six different donors.

(C) Immunofluorescence staining of TLR4 in PBMCs treated with formulation control or inactivated H5N1. TLR4 was distributed throughout the cytoplasm in control cells (top). PBMCs treated with inactivated H5N1 showed peripheralization of TLR4 (bottom).

(D) Lung elastance in WT and ncf1−/− mice following intratracheal administration of inactivated H5N1 viruses. n = 4 for each group. ∗∗p < 0.01 for the whole time course.

(E) Lung pathology (top; H&E staining) and immunolocalization of oxidized PLs (bottom) in lung tissue of H5N1-challenged WT and ncf1−/− mice. Original magnifications × 200.

(F) Immunohistochemistry of OxPLs in lungs from two patients infected with H5N1 avian influenza virus (top) and two patients infected with SARS-coronavirus (bottom).

(G) Immunohistochemistry of OxPLs in rhesus monkeys and rabbits infected with Bacillus anthracis (left panels) and Cynomolgus monkeys infected with Monkey Pox or Yersinia pestis (right). In (F) and (G), OxPLs detected by the mAb EO6 were seen in inflammatory exudates lining the injured alveoli (arrows) and macrophages (triangles). Original magnifications × 400. Data are mean values ± SEM.