This study was conducted to investigate annexin A1 (ANXA1) functions in human placental explants infected with Toxoplasma gondii (T. gondii). We examined the first and third trimester placental explants infected with T. gondii (n = 7 placentas/group) to identify the number and location of parasites, ANXA1 protein, potential involvement of formyl peptide receptors (FPR1 and FPR2), and COX-2 expressions by immunohistochemistry. Treatments with Ac2-26mimetic peptide of ANXA1 were performed to verify the parasitism rate (β-galactosidase assay), prostaglandin E2levels (ELISA assay), and ANXA1, FPR1 and COX-2 expression in third trimester placentas. Placental explants of third trimester expressed less ANXA1 and were more permissive to T. gondii infection than first trimester placentas that expressed more ANXA1. Ac2-26treatment increases endogenous ANXA1 and decreases parasitism rate, COX-2, and prostaglandin E2levels. Altogether, these data provide further insight into the anti-parasitic and anti-inflammatory effects of ANXA1 in placentas infected with T. gondii.
de Oliveira Cardoso, M.F., Moreli, J.B., Gomes, A.O., de Freitas Zanon, C., Silva, A.E., Ricci, L., et al. (2018). Annexin A1 peptide is able to induce an anti-parasitic effect in human placental explants infected by Toxoplasma gondii. MICROBIAL PATHOGENESIS, 123, 153-161 [10.1016/j.micpath.2018.07.005].
Annexin A1 peptide is able to induce an anti-parasitic effect in human placental explants infected by Toxoplasma gondii
Ricci, Luana;Ietta, Francesca;
2018-01-01
Abstract
This study was conducted to investigate annexin A1 (ANXA1) functions in human placental explants infected with Toxoplasma gondii (T. gondii). We examined the first and third trimester placental explants infected with T. gondii (n = 7 placentas/group) to identify the number and location of parasites, ANXA1 protein, potential involvement of formyl peptide receptors (FPR1 and FPR2), and COX-2 expressions by immunohistochemistry. Treatments with Ac2-26mimetic peptide of ANXA1 were performed to verify the parasitism rate (β-galactosidase assay), prostaglandin E2levels (ELISA assay), and ANXA1, FPR1 and COX-2 expression in third trimester placentas. Placental explants of third trimester expressed less ANXA1 and were more permissive to T. gondii infection than first trimester placentas that expressed more ANXA1. Ac2-26treatment increases endogenous ANXA1 and decreases parasitism rate, COX-2, and prostaglandin E2levels. Altogether, these data provide further insight into the anti-parasitic and anti-inflammatory effects of ANXA1 in placentas infected with T. gondii.File | Dimensione | Formato | |
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https://hdl.handle.net/11365/1055775