Figure 4
From: Critical role of CXCL4 in the lung pathogenesis of influenza (H1N1) respiratory infection
Chemokine (C-X-C motif) ligand 4 (CXCL4) knockout alters the accumulation of bronchoalveolar lavage fluid (BALF) immunocytes without affecting activation of lung adaptive immunity after H1N1 influenza virus infection. Wild-type (WT) and CXCL4−/− mice were infected with H1N1 influenza virus (2,000 CCID50) (50% cell culture infective dose) on day 0, and the BALF and lymphocytes from the lung-draining mediastinal lymph node of the infected mice were collected and analyzed at the indicated time points postinfection. (a) The total number of leukocytes in the BALF was counted. (b–d) The total number of macrophages (b), neutrophils (c) and lymphocytes (d) was determined. (e) The total number of CD4+ T cells, CD8+ T cells, and CD19+ B cells in the mediastinal lymph nodes at 9 days postinfection (d.p.i.) were determined by flow cytometry. (f) The percentage of CD8+ and interferon (IFN)-γ+ cells in the mediastinal lymph node lymphocytes collected at 9 d.p.i. was determined by flow cytomtery. (g) The levels of the T helper type 1 (Th1) and Th2 effector cytokines IFN-γ, interleukin (IL)-4, IL-5, and IL-10 were measured using the Bio-Plex Mouse Cytokine Th1/Th2 Assay. (h) The sera of infected mice were collected at 9 d.p.i., and the hemagglutination inhibition titers of the sera against H1N1 A/PR/8 were evaluated. Error bars represent the s.d. of four samples. *P<0.05 based on Student’s t-test.
