Fig. 8.
C57BL/6 wild-type (WT) and interferon-α receptor knockout (IFNAR KO) mice were inoculated intranasally with 40 plaque-forming units A/PR/8/34 influenza virus day 0 postviral infection (PVI) and exposed to 2.5 × 106 colony-forming units (CFU) EF3030 (day 6 PVI) and killed and harvested (24 h postbacterial infection [PBI]). Halothane-exposed mice (white bars) were exposed to 2% halothane for 2 h just before infection (day 0) and again for 2 h on day 4 PVI. Nonhalothane-exposed mice (black bars) received ketamine sedation. (A) Bronchoalveolar lavage (BAL; albumin) and (B) total lung EF3030 burden were determined. Sample sizes are displayed above groups. **P < 0.01 WT or IFNAR KO halothane–exposed mice compared with their nonhalothane-exposed control of their respective genetic background. Data are expressed as mean ± SEM. EF3030 = Streptococcus pneumoniae.

C57BL/6 wild-type (WT) and interferon-α receptor knockout (IFNAR KO) mice were inoculated intranasally with 40 plaque-forming units A/PR/8/34 influenza virus day 0 postviral infection (PVI) and exposed to 2.5 × 106 colony-forming units (CFU) EF3030 (day 6 PVI) and killed and harvested (24 h postbacterial infection [PBI]). Halothane-exposed mice (white bars) were exposed to 2% halothane for 2 h just before infection (day 0) and again for 2 h on day 4 PVI. Nonhalothane-exposed mice (black bars) received ketamine sedation. (A) Bronchoalveolar lavage (BAL; albumin) and (B) total lung EF3030 burden were determined. Sample sizes are displayed above groups. **P < 0.01 WT or IFNAR KO halothane–exposed mice compared with their nonhalothane-exposed control of their respective genetic background. Data are expressed as mean ± SEM. EF3030 = Streptococcus pneumoniae.

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