Nonimmune Cells Contribute to Crosstalk between Immune Cells and Inflammatory Mediators in the Innate Response to Trypanosoma cruzi Infection
Figure 3
Comparative analysis of hepatic injury, inflammation and TLR expression in Trypanosoma cruzi-infected B6 and BALB/c mice. The parasitemia was higher in BALB/c than B6 mice. However infected B6 mouse strain showed stronger and injurious inflammatory environment (increased NO and ROS) associated with high levels of TLR2, TLR4, and TLR9 in hepatic leukocytes. In contrast, BALB/c mice displayed more balanced proinflammatory/immunoregulatory cytokines profile during the acute infection. Furthermore, TLR2 and TLR4 were upregulated in infiltrating leukocytes and hepatocytes as well, while TLR9 expression was low in hepatic leukocytes of infected BALB/c mice. Altogether the results suggested that the strong inflammatory environment elicited in infected B6 mice plus the loss of TLR2 signaling may be responsible for the severity of the hepatic injury and higher mortality of this mouse strain [19, 23].
