Fig. 3.
Fig. 3. The increase in IFN-γ, IL-18, and IL-12 levels in the lungs stimulated by pulmonary adenovirus infection is severely impaired in GM−/− mice. / (A) BAL fluid was collected from GM+/+, GM−/−, and SPC-GM+/+/GM−/− mice 36 hours after pulmonary adenovirus infection and evaluated for the presence of IFN-γ by ELISA. Asterisks indicate that no IFN-γ was detected in the lungs of any mice in the absence of adenovirus lung infection. Data represent means ± SEM; n = 4 (GM−/− or SPC-GM+/+/GM−/−) or n = 3 (GM+/+) mice per group; BAL fluid from each mouse was analyzed individually. Differences in IFN-γ levels in infected (+) and uninfected (−) GM+/+ and SPC-GM+/+/GM−/− mice were significant (P < .02) but were not significant in GM−/−mice (P = .10). (B) Mice exposed to adenovirus as above were also evaluated for the presence of IL-18 in BAL. IL-18 levels in BAL fluid of infected animals are shown. Data represent the means ± SEM; n = 6 (GM−/− or SPC-GM+/+/GM−/−) or n = 3 (GM+/+) mice per group; BAL fluid from each mouse was analyzed individually. IL-18 was not detected in BAL fluid from adenovirus-exposed GM−/− mice (*). Differences in IL-18 levels in GM+/+ and GM−/− mice were significant (P < .05). The adenovirus-simulated increase in IL-18 levels in the lungs was restored in SPC-GM+/+/GM−/− mice. (C) The same animals evaluated in panel A were also evaluated for the presence of IL-12 in BAL. IL-12 levels in BAL fluid of infected animals are shown. Data represent the means ± SEM; n = 7 mice per group. Differences in IL-12 levels in GM+/+ and GM−/− mice were significant (P < .05). The adenovirus-simulated increase in IL-18 levels in the lungs was restored in SPC-GM+/+/GM−/− mice.

The increase in IFN-γ, IL-18, and IL-12 levels in the lungs stimulated by pulmonary adenovirus infection is severely impaired in GM−/− mice.

(A) BAL fluid was collected from GM+/+, GM−/−, and SPC-GM+/+/GM−/− mice 36 hours after pulmonary adenovirus infection and evaluated for the presence of IFN-γ by ELISA. Asterisks indicate that no IFN-γ was detected in the lungs of any mice in the absence of adenovirus lung infection. Data represent means ± SEM; n = 4 (GM−/− or SPC-GM+/+/GM−/−) or n = 3 (GM+/+) mice per group; BAL fluid from each mouse was analyzed individually. Differences in IFN-γ levels in infected (+) and uninfected (−) GM+/+ and SPC-GM+/+/GM−/− mice were significant (P < .02) but were not significant in GM−/−mice (P = .10). (B) Mice exposed to adenovirus as above were also evaluated for the presence of IL-18 in BAL. IL-18 levels in BAL fluid of infected animals are shown. Data represent the means ± SEM; n = 6 (GM−/− or SPC-GM+/+/GM−/−) or n = 3 (GM+/+) mice per group; BAL fluid from each mouse was analyzed individually. IL-18 was not detected in BAL fluid from adenovirus-exposed GM−/− mice (*). Differences in IL-18 levels in GM+/+ and GM−/− mice were significant (P < .05). The adenovirus-simulated increase in IL-18 levels in the lungs was restored in SPC-GM+/+/GM−/− mice. (C) The same animals evaluated in panel A were also evaluated for the presence of IL-12 in BAL. IL-12 levels in BAL fluid of infected animals are shown. Data represent the means ± SEM; n = 7 mice per group. Differences in IL-12 levels in GM+/+ and GM−/− mice were significant (P < .05). The adenovirus-simulated increase in IL-18 levels in the lungs was restored in SPC-GM+/+/GM−/− mice.

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