ArticleMolecular and cellular biochemistry2000
Toxoplasma gondii induces the secretion of monocyte chemotactic protein-1 in human fibroblasts, in vitro.
Article in Molecular and cellular biochemistry, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 30 citations in OpenAlex.
- Inhibitory Effects ofEvidence-based complementary and alternative medicine : eCAM · 2021Article
- Computational Reconstruction of NFκB Pathway Interaction Mechanisms during Prostate Cancer.PLoS computational biology · 2016Article
- Long-Term Relationships: the Complicated Interplay between the Host and the Developmental Stages of Toxoplasma gondii during Acute and Chronic Infections.Microbiology and molecular biology reviews : MMBR · 2015Review
- Lack of a Functioning P2X7 Receptor Leads to Increased Susceptibility to Toxoplasmic Ileitis.PloS one · 2015Article
- Recurrent headaches may be caused by cerebral toxoplasmosis.World journal of clinical pediatrics · 2014Article
- GRA25 is a novel virulence factor of Toxoplasma gondii and influences the host immune response.Infection and immunity · 2014Article
- The role of DNA microarrays in Toxoplasma gondii research, the causative agent of ocular toxoplasmosis.Journal of ocular biology, diseases, and informatics · 2009Article
- Monocyte-mediated defense against microbial pathogens.Annual review of immunology · 2008Review
- Involvement of MAPK activation in chemokine or COX-2 productions by Toxoplasma gondii.The Korean journal of parasitology · 2006Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Secretion of Monocyte Chemotactic Protein-1 (MCP-1) by fibroblasts infected with Toxoplasma gondii was studied in vitro. A significantly higher MCP-1 secretion was observed 24 h after infection by live tachyzoites. Analysis of chemokine mRNA transcripts by RNase protection assay revealed that this MCP-1 secretion seems associated with increased MCP-1 mRNA expression. However, these increased levels of MCP-1 secretion and expression were not obtained after stimulation by heat-killed tachyzoites or parasites pre-treated by a specific inhibitor of phosphatidylcholine-specific phospholipase C (D609). Inhibition of parasite multiplication by pyrimethamine did not modify MCP-1 secretion. Thus, it appeared that the active penetration of T. gondii in cells was of major importance in the induction of MCP-1 secretion. None of the other chemokines studied by RNase protection assay (lymphotactin, RANTES, IP-10, MIP-1alpha, MIP-1beta, IL-8, and I-309) were expressed after infection by live tachyzoites. We also found that MCP-1 secretion induced by live T. gondii is blocked by inhibitors of nuclear factor (NF)-kappaB activation, ALLN and MG132. Such data indicate that NF-kappaB could be involved in T. gondii-induced MCP-1 production. MCP-1 secretion may contribute to the recruitment of monocytes and lymphocytes and thus participate in the control of T. gondii infection and in its pathogenesis.
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