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. 2018 Dec;59(6):770–781. doi: 10.1165/rcmb.2018-0004OC

Figure 1.

Figure 1.

Cigarette smoke (CS) exposure leads to a heightened inflammatory response, delayed recovery of body weight, and an initial modest increase in viral titers after influenza infection. Mice preexposed to smoke were infected with ∼10 plaque-forming units (pfu) of influenza A virus and continued to get smoke exposure until they were killed at different time points. (A) Total number of inflammatory cells in the BAL of mice. (B–D) Numbers of neutrophils (B), macrophages (C), and lymphocytes (D) in the BAL of influenza-infected mice with or without CS exposure. (E) Recovery of weight was delayed in the CS group, and the difference between the CS and nonsmoking (NS) groups became significant from Day 27 after infection. (F) The levels of influenza A virus mRNA were higher in the lung homogenates of CS-exposed mice on Day 3 after infection, but there was no significant difference between the two groups after Day 6. Data are from one of at least three independent experiments performed with n = 4–6 in each group at each given time point. *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001 comparing CS and NS groups at the same time point. WBC = white blood cell.