<i>Toxoplasma gondii</i>Cyclophilin 18 Regulates the Proliferation and Migration of Murine Macrophages and Spleen Cells

Ibrahim, Hany M.; Xuan, Xuenan; Nishikawa, Yoshifumi

doi:10.1128/cvi.00128-10

Cited by 30 publications

(33 citation statements)

References 44 publications

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“…Additionally, there was no significant difference in the recruitment of CD11b + cells between WT and CCR5 −/− mice that were infected peritoneally with RH-GFP tachyzoites. Recently, our group demonstrated that recombinant TgCyp18 controlled the in vitro migration of macrophages and lymphocytes in CCR5-dependent and -independent ways [14]. Therefore, the results presented here suggest that the TgCyp18-induced cell migration occurred in a CCR5-independent way in our in vivo experimental model.…”

Section: Discussionsupporting

confidence: 65%

Overproduction of Toxoplasma gondii cyclophilin-18 regulates host cell migration and enhances parasite dissemination in a CCR5-independent manner

et al. 2014

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BackgroundToxoplasma gondii hijacks host cells to allow it to disseminate throughout a host animal; however, the migratory machinery involved in this process has not been well characterized. We examined the functional role of T. gondii cyclophilin 18 (TgCyp18) in host cell recruitment using recombinant parasites transfected with TgCyp18.ResultsHigh levels of TgCyp18 enhanced IL-12 production in cysteine-cysteine chemokine receptor 5 (CCR5) knockout mice (CCR5−/−) that had been infected peritoneally with T. gondii. Recruitment of CD11b+ cells to the infection site was enhanced in a CCR5-independent manner. T. gondii spread to several organs, particularly the liver, in a TgCyp18-dependent and CCR5-independent manner. Additionally, CCL5 levels were upregulated in macrophages treated with recombinant protein TgCyp18 and in the peritoneal fluids of the infected CCR5−/− mice. Furthermore, the chemokines involved in macrophage migration, CCL2 and CXCL10, were upregulated in the livers of CCR5−/− mice infected with recombinant parasites that had been transfected with TgCyp18.ConclusionTgCyp18 may play a crucial role in macrophage migration, and in assisting with transport of T. gondii via CCR5-independent mechanisms. TgCyp18 may also play a role with CCL5 in the migration of macrophages to the site of infection, and with CCL2 and CXCL10 in the transport of T. gondii-infected cells to the liver.

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Section: Discussionsupporting

confidence: 65%

Overproduction of Toxoplasma gondii cyclophilin-18 regulates host cell migration and enhances parasite dissemination in a CCR5-independent manner

et al. 2014

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“…The extracellular form of Toxoplasma gondii ’s adhesin MIC2 interacts with host ICAM-1 to initiate the free parasite to cross epithelial barriers made up of human foreskin fibroblast (HFF) cell monolayers 20 , 21 . In order to cross the BBB as an intracellular parasite Toxoplasma gondii secreted cyclophilin 18 interacts with the chemokine receptor CCR5 and attracts WBCs to the site of infection 36 , 37 . Toxoplasma gondii derived proteases process and shed parasite-derived proteins necessary for the penetration into the host cell.…”

Section: Discussionmentioning

confidence: 99%

Passage of parasites across the blood-brain barrier

Masocha

Kristensson

2012

Virulence

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The blood-brain barrier (BBB) is a structural and functional barrier that protects the central nervous system (CNS) from invasion by blood-borne pathogens including parasites. However, some intracellular and extracellular parasites can traverse the BBB during the course of infection and cause neurological disturbances and/or damage which are at times fatal. The means by which parasites cross the BBB and how the immune system controls the parasites within the brain are still unclear. In this review we present the current understanding of the processes utilized by two human neuropathogenic parasites, Trypanosoma brucei spp and Toxoplasma gondii, to go across the BBB and consequences of CNS invasion. We also describe briefly other parasites that can invade the brain and how they interact with or circumvent the BBB. The roles played by parasite-derived and host-derived molecules during parasitic and white blood cell invasion of the brain are discussed.

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“…On the other hand, the parasite adapts to this by differentiating from tachyzoites into bradyzoites (161). Apart from this, TgCyp18 at high concentrations enhances the proliferation of macrophages and spleen cells, in a CCR5-independent manner, while the migration of these cells toward the infection site is dependent on the interaction between CCR5 and TgCyp18 (162).…”

Section: Protozoan Ppiases In Virulencementioning

confidence: 99%

Microbial Peptidyl-Prolyl cis / trans Isomerases (PPIases): Virulence Factors and Potential Alternative Drug Targets

Ünal

Steinert

2014

Microbiol Mol Biol Rev

154

146

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SUMMARY Initially discovered in the context of immunomodulation, peptidyl-prolyl cis/trans isomerases (PPIases) were soon identified as enzymes catalyzing the rate-limiting protein folding step at peptidyl bonds preceding proline residues. Intense searches revealed that PPIases are a superfamily of proteins consisting of three structurally distinguishable families with representatives in every described species of prokaryote and eukaryote and, recently, even in some giant viruses. Despite the clear-cut enzymatic activity and ubiquitous distribution of PPIases, reports on solely PPIase-dependent biological roles remain scarce. Nevertheless, they have been found to be involved in a plethora of biological processes, such as gene expression, signal transduction, protein secretion, development, and tissue regeneration, underscoring their general importance. Hence, it is not surprising that PPIases have also been identified as virulence-associated proteins. The extent of contribution to virulence is highly variable and dependent on the pleiotropic roles of a single PPIase in the respective pathogen. The main objective of this review is to discuss this variety in virulence-related bacterial and protozoan PPIases as well as the involvement of host PPIases in infectious processes. Moreover, a special focus is given to Legionella pneumophila macrophage infectivity potentiator (Mip) and Mip-like PPIases of other pathogens, as the best-characterized virulence-related representatives of this family. Finally, the potential of PPIases as alternative drug targets and first tangible results are highlighted.

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Toxoplasma gondiiCyclophilin 18 Regulates the Proliferation and Migration of Murine Macrophages and Spleen Cells

Cited by 30 publications

References 44 publications

Overproduction of Toxoplasma gondii cyclophilin-18 regulates host cell migration and enhances parasite dissemination in a CCR5-independent manner

Overproduction of Toxoplasma gondii cyclophilin-18 regulates host cell migration and enhances parasite dissemination in a CCR5-independent manner

Passage of parasites across the blood-brain barrier

Microbial Peptidyl-Prolyl cis / trans Isomerases (PPIases): Virulence Factors and Potential Alternative Drug Targets

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