Lipid Bodies: Inflammatory Organelles Implicated in Host-Trypanosoma cruzi Interplay during Innate Immune Responses
Figure 6
Uptake of apoptotic cells by macrophages induces lipid body formation and PGE2 synthesis during Trypanosoma cruzi infection. LB formation (a) and prostaglandin E2 (PGE2) synthesis (b) by mice macrophages infected in vitro with T. cruzi alone or co-cultured with apoptotic cells for 24 hours. Each bar represents the mean ± standard error of the mean (SEM) from 50 consecutively counted macrophages from at least 4 independent pools of 3 animals each. Statistically significant (P # 0.05) differences between control and infected or stimulated groups are indicated by asterisks; M, macrophages. In (c), a large typical apoptotic body (outlined in red in (ci)) showing very condensed, electron-dense nuclear chromatin and degenerating mitochondria (red arrowheads) is seen within a heart macrophage of a rat with 12 days of infection. Note that the apoptotic body is surrounded by several lipid bodies with distinct electron densities. Rats were infected with the Y strain of T. cruzi and the myocardium processed for transmission electron microscopy at day 12 of the acute infection. Reprinted from [35] with permission. Scale bar, 1 μm.
