TNF-α is a critical negative regulator of type 1 immune activation during intracellular bacterial infection
J. Clin. Invest. Anna Zganiacz, et al. 113:401 doi:10.1172/JCI18991 [Go to this article.]

Figure 1
(a) Mortality of TNF^–/– mice following infection by rBCG. Both B6-WT and TNF^–/– mice were infected intratracheally with rBCG, and the mortality of the mice was monitored thereafter. Results are from 15–20 mice per group, representative of more than two experiments. (b and c) Tissue level of mycobacterial infection. Infected B6-WT and TNF^–/– mice were sacrificed at days 14, 27, and 37, and their lungs (b) and spleens (c) were homogenized and evaluated by using a colony enumeration assay. Results are expressed as mean ± SEM from 6–12 mice per group per time. The difference between B6-WT and TNF^–/– at both days 27 and 37 is statistically very significant (P ≤ 0.01). (d) Hemoglobin oxygen saturation in the peripheral blood over the course of pulmonary mycobacterial infection. At various time points, the percentage of oxygen saturation of hemoglobin was measured on live mice by using a veterinary oximeter. Results are expressed as mean ± SEM from 5–10 mice per group per time point.