diminazene aceturate (berenil) modulates the host cellular and inflammatory responses to trypanosoma congolense infectiondiminazene aceturate(berenil)调节宿主细胞和炎性反应锥虫属congolense感染.pdfVIP

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diminazene aceturate (berenil) modulates the host cellular and inflammatory responses to trypanosoma congolense infectiondiminazene aceturate(berenil)调节宿主细胞和炎性反应锥虫属congolense感染.pdf

diminazene aceturate (berenil) modulates the host cellular and inflammatory responses to trypanosoma congolense infectiondiminazene aceturate(berenil)调节宿主细胞和炎性反应锥虫属congolense感染

Diminazene Aceturate (Berenil) Modulates the Host Cellular and Inflammatory Responses to Trypanosoma congolense Infection . . Shiby Kuriakose , Helen M. Muleme , Chukwunonso Onyilagha, Rani Singh, Ping Jia, Jude E. Uzonna* Department of Immunology, University of Manitoba, Winnipeg, Manitoba, Canada Abstract Background: Trypanosoma congolense are extracellular and intravascular blood parasites that cause debilitating acute or chronic disease in cattle and other domestic animals. Diminazene aceturate (Berenil) has been widely used as a chemotherapeutic agent for trypanosomiasis in livestock since 1955. As in livestock, treatment of infected highly susceptible BALB/c mice with Berenil leads to rapid control of parasitemia and survival from an otherwise lethal infection. The molecular and biochemical mechanisms of action of Berenil are still not very well defined and its effect on the host immune system has remained relatively unstudied. Here, we investigated whether Berenil has, in addition to its trypanolytic effect, a modulatory effect on the host immune response to Trypanosoma congolense. Methodology/Principal Findings: BALB/c and C57BL/6 mice were infected intraperitoneally with T. congolense, treated with Berenil and the expression of CD25 and FoxP3 on splenic cells was assessed directly ex vivo. In addition, serum levels and spontaneous and LPS-induced production of pro-inflammatory cytokines by splenic and hepatic CD11b+ cells were determined by ELISA. Berenil treatment significantly reduced the percentages of CD25+ cells, a concomitant reduction in the percentage of regulatory (CD4+ +

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