Trypanosoma cruzi is a parasite with large amounts of sialic acid (SA) residues exposed at its surface that seems to be involved in macrophages infection. Some macrophages, present in T. cruzi infected tissues, expresses sialoadhesin (Sn), a receptor that recognizes SA. Thus, the involvement of Sn in the association of T. cruzi to macrophages was investigated. Sn was induced in mice peritoneal macrophages by homologous serum (HS) cultivation. Epimastigotes and trypomastigotes associated more to HS cultured macrophages than to fetal bovine serum (FBS). Blocking of Sn with antibodies reduced the association of trypomastigotes to similar level as for FBS cultured macrophages. Desialylation reduced the association of parasites to HS cultured macrophages indicating the Sn importance. Furthermore, the entrance mechanism of trypomastigotes to Sn positive macrophages has a phagocytic nature as demonstrated by scanning electron microscopy and cytochalasin D treatment. Sn positive macrophages may important in the initial trypomastigote infection, thus in the establishment of Chagas disease.

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Lipid bodies [lipid droplets (LBs)] are lipid-rich organelles involved in lipid metabolism, signalling and inflammation. Recent findings suggest a role for LBs in host response to infection; however, the potential functions of this organelle in Toxoplasma gondii infection and how it alters macrophage microbicidal capacity during infection are not well understood. Here, we investigated the role of host LBs in T. gondii infection in mouse peritoneal macrophages in vitro. Macrophages cultured with mouse serum (MS) had higher numbers of LBs than those cultured in foetal bovine serum and can function as a model to study the role of LBs during intracellular pathogen infection. LBs were found in association with the parasitophorous vacuole, suggesting that T. gondii may benefit from this lipid source. Moreover, increased numbers of macrophage LBs correlated with high prostaglandin E2 (PGE2) production and decreased nitric oxide (NO) synthesis. Accordingly, LB-enriched macrophages cultured with MS were less efficient at controlling T. gondii growth. Treatment of macrophages cultured with MS with indomethacin, an inhibitor of PGE2 production, increased the microbicidal capacity against T. gondii. Collectively, these results suggest that culture with MS caused a decrease in microbicidal activity of macrophages against T. gondii by increasing PGE2 while lowering NO production.

Tachyzoites of Toxoplasma gondii are able to infect several cell types tested (wild-type chinese hamster ovary (CHO) cells and glycosylation mutants, Vero and LLCMK2 cells). However, the extent of infection varied. Mutant cells which present few or no surface-exposed sialic acid residues were infected to a lower extent. Similar results were obtained if sialic acid residues were removed by previous neuraminidase treatment. Addition of sialic acid residues to surface-exposed glycoconjugates using fetuin as a sialic acid donor and the trans-sialidase of Trypanosoma cruzi rendered the cells more easily infected by Toxoplasma gondii. These observations indicate that surface-exposed carbohydrate residues of the host cell are involved on the process of Toxoplasma gondii-host cell recognition.