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Culture of mouse peritoneal macrophages with mouse serum induces lipid bodies that associate with the parasitophorous vacuole and decrease their microbicidal capacity against Toxoplasma gondii
Authors:Laura Azeredo Miranda Mota  Jo?o Roberto  Neto   Ver?nica Gomes Monteiro  Caroliny Samary Silva Lobato  Marco Antonio de Oliveira  Maura da Cunha  Heloisa D’ávila  Sérgio Henrique Seabra  Patrícia Torres Bozza  Renato Augusto DaMatta
Abstract:Lipid bodies [lipid droplets (LBs)] are lipid-rich organelles involved in lipidmetabolism, signalling and inflammation. Recent findings suggest a role for LBs inhost response to infection; however, the potential functions of this organellein Toxoplasma gondii infection and how it alters macrophagemicrobicidal capacity during infection are not well understood. Here, we investigatedthe role of host LBs in T. gondii infection in mouse peritonealmacrophages in vitro. Macrophages cultured with mouse serum (MS) had higher numbersof LBs than those cultured in foetal bovine serum and can function as a model tostudy the role of LBs during intracellular pathogen infection. LBs were found inassociation with the parasitophorous vacuole, suggesting that T. gondiimay benefit from this lipid source. Moreover, increased numbers ofmacrophage LBs correlated with high prostaglandin E2 (PGE2) production and decreasednitric oxide (NO) synthesis. Accordingly, LB-enriched macrophages cultured with MSwere less efficient at controlling T. gondii growth. Treatment ofmacrophages 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 activityof macrophages against T. gondii by increasing PGE2 while loweringNO production.
Keywords:macrophages   lipid bodies   nitric oxide   prostaglandin   microbicidal capacity   Toxoplasma gondii
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