Characterization of Plasmodium berghei Homologues of T-cell Immunomodulatory Protein as a New Potential Candidate for Protecting against Experimental Cerebral Malaria
2
조회
0
다운로드
0
인용
0
참고문헌
키워드
초록
The pathogenesis of cerebral malaria is biologically complex and involves multi-factorial mechanisms such as mi- crovascular congestion, immunopathology by the pro-inflammatory cytokine and endothelial dysfunction. Recent data have suggested that a pleiotropic T-cell immunomodulatory protein (TIP) could effectively mediate inflammatory cytokines of mammalian immune response against acute graft-versus-host disease in animal models. In this study, we identified a con- served homologue of TIP in Plasmodium berghei (PbTIP) as a membrane protein in Plasmodium asexual stage. Compared with PBS control group, the pathology of experimental cerebral malaria (ECM) in rPbTIP intravenous injection (i.v.) group was alleviated by the downregulation of pro-inflammatory responses, and rPbTIP i.v. group elicited an expansion of regulatory T- cell response. Therefore, rPbTIP i.v. group displayed less severe brain pathology and feverish mice in rPbTIP i.v. group died from ECM. This study suggested that PbTIP may be a novel promising target to alleviate the severity of ECM.
Abstract
The pathogenesis of cerebral malaria is biologically complex and involves multi-factorial mechanisms such as mi- crovascular congestion, immunopathology by the pro-inflammatory cytokine and endothelial dysfunction. Recent data have suggested that a pleiotropic T-cell immunomodulatory protein (TIP) could effectively mediate inflammatory cytokines of mammalian immune response against acute graft-versus-host disease in animal models. In this study, we identified a con- served homologue of TIP in Plasmodium berghei (PbTIP) as a membrane protein in Plasmodium asexual stage. Compared with PBS control group, the pathology of experimental cerebral malaria (ECM) in rPbTIP intravenous injection (i.v.) group was alleviated by the downregulation of pro-inflammatory responses, and rPbTIP i.v. group elicited an expansion of regulatory T- cell response. Therefore, rPbTIP i.v. group displayed less severe brain pathology and feverish mice in rPbTIP i.v. group died from ECM. This study suggested that PbTIP may be a novel promising target to alleviate the severity of ECM.
참고문헌 (51)
- World Malaria Report, 2018, "World Health Organization", World Health Organization, ~ (2018)
- White NJ, "Malaria", Lancet, 383, pp.723~735 (2014)
- John CC, "Cerebral malaria in children is associated with long-term cognitive impairment", Pediatrics, 122, pp.92~99 (2008)
- MacCormick IJC, "Cerebral malaria in children : using the retina to study the brain", Brain, 137, pp.2119~2142 (2014)
- Guo J, "Reduction of experimental cerebral malaria and its related proinflammatory responses by the novel liposome-based β-methasone nanodrug", Biomed Res Int, 2014, pp.66~70 (2014)
- Khandare AV, "Expression of negative immune regulatory molecules, pro-inflammatory chemokine and cytokines in immunopathology of ECM developing mice", Acta Trop, 172, pp.58~63 (2017)
- Dunst J, "Cytokines and Chemokines in Cerebral Malaria Pathogenesis", Front Cell Infect Microbiol, 7, pp.324~ (2017)
- Mathieu C, "Plasmodium berghei histamine-releasing factor favours liver-stage development via inhibition of IL-6 production and associates with a severe outcome of disease", Cell Microbiol, 17, pp.542~558 (2015)
- Keita Alassane S, "Young Sprague Dawley rats infected by Plasmodium berghei : A relevant experimental model to study cerebral malaria", PLoS One, 12, pp.e0181300~ (2017)
- Pino P, "Plasmodium falciparum--infected erythrocyte adhesion induces caspase activation and apoptosis in human endothelial cells", J Infect Dis, 187, pp.1283~1290 (2003)
- Fiscella M, "TIP, a T-cell factor identified using high-throughput screening increases survival in a graft-versus-host disease model", Nat Biotechnol, 21, pp.302~307 (2003)
- Nono JK, "EmTIP, a T-Cell Immunomodulatory Protein Secreted by the Tapeworm Echinococcus multilocularis Is Important for Early Metacestode Development", PLoS Neglect Trop Dis, 8, pp.e2632~ (2014)
- Blagborough AM, "Plasmodium berghei HAP2 induces strong malaria transmission-blocking immunity in vivo and in vitro", Vaccine, 27, pp.5187~5194 (2009)
- Chan JA, "Surface antigens of Plasmodium falciparum-infected erythrocytes as immune targets and malaria vaccine candidates", Cell Mol Life Sci, 71, pp.3633~3657 (2014)
- Dempsey E, "Antimitotic herbicides bind to an unidentified site on malarial parasite tubulin and block development of liver-stage Plasmodium parasites", Mol Biochem Parasit, 188, pp.116~127 (2013)
- Deligianni E, "Critical role for a stage-specific actin in male exflagellation of the malaria parasite", Cell Microbiol, 13, pp.1714~1730 (2011)
- Eisenhaber B, "Enzymes and auxiliary factors for GPI lipid anchor biosynthesis and post-translational transfer to proteins", Bioessays, 25, pp.367~385 (2003)
- Baccarella A, "Loss of Toll-like receptor 7 alters cytokine production and protects against experimental cerebral malaria", Malaria J, 13, pp.354~ (2014)
- He X, "Vitamin D inhibits the occurrence of experimental cerebral malaria in mice by suppressing the host inflammatory response", J Immunol, 193, pp.1314~1323 (2014)
- Mlambo G, "Functional immunogenicity of baculovirus expressing Pfs25, a human malaria transmission-blocking vaccine candidate antigen", Vaccine, 28, pp.7025~7029 (2010)
- Kumar R, "Nanovaccines for malaria using Plasmodium falciparum antigen Pfs25 attached gold nanoparticles", Vaccine, 33, pp.5064~5071 (2015)
- Wei X, "Erythropoietin protects against murine cerebral malaria through actions on host cellular immunity", Infect Immun, 82, pp.165~173 (2014)
- Yamakuchi M, "Antibody to human leukocyte antigen triggers endothelial exocytosis", Proc Natl Acad Sci USA, 104, pp.1301~1306 (2007)
- Wahl SM, "Regulatory T cells and transcription factors : gatekeepers in allergic inflammation", Curr Opin Immunol, 16, pp.768~774 (2004)
- Sakaguchi S, "Naturally arising CD4+ regulatory t cells for immunologic self-tolerance and negative control of immune responses", Annu Rev Immunol, 22, pp.531~562 (2004)
- Sakaguchi S, "Naturally arising Foxp3-expressing CD25+CD4+ regulatory T cells in immunological tolerance to self and non-self", Nat Immunol, 6, pp.345~352 (2005)
- McHugh RS, "CD4+CD25+ immunoregulatory T cells : gene expression analysis reveals a functional role for the glucocorticoid-induced TNF receptor", Immunity, 16, pp.311~323 (2002)
- Chen W, "Engagement of cytotoxic T lymphocyte–associated antigen 4(CTLA-4)induces transforming growth factor β(TGF-β)production by murine CD4 T Cells", J Exp Med, 188, pp.1849~1857 (1998)
- Fontenot JD, "Foxp3 programs the development and function of CD4+CD25+ regulatory T cells", Nat Immunol, 4, pp.330~336 (2003)
- Khattri R, "An essential role for Scurfin in CD4+CD25+ T regulatory cells", Nat Immunol, 4, pp.337~342 (2003)
- Hori S, "Control of regulatory T cell development by the transcription factor Foxp3", Science, 299, pp.1057~1061 (2003)
- Amani V, "Involvement of IFN-gamma receptor-medicated signaling in pathology and anti-malarial immunity induced by Plasmodium berghei infection", Eur J Immunol, 30, pp.1646~ (2000)
- Belnoue E, "Control of pathogenic CD8+ T cell migration to the brain by IFN-gamma during experimental cerebral malaria", Parasite Immunol, 30, pp.544~553 (2010)
- Grau GE, "Monoclonal antibody against interferon gamma can prevent experimental cerebral malaria and its associated overproduction of tumor necrosis factor", Proc Natl Acad Sci USA, 86, pp.5572~5574 (1989)
- Turner GD, "An immunohistochemical study of the pathology of fatal malaria. Evidence for widespread endothelial activation and a potential role for intercellular adhesion molecule-1 in cerebral sequestration", Am J Pathol, 145, pp.1057~1069 (1994)
- Roberts DJ, "Autoagglutination of malaria-infected red blood cells and malaria severity", Lancet, 355, pp.1427~1428 (2000)
- Rénia L, "Cerebral malaria : mysteries at the blood-brain barrier", Virulence, 3, pp.193~201 (2012)
- Medana IM, "Human cerebral malaria and the blood-brain barrier", Int J Parasitol, 36, pp.555~568 (2006)
- Turner GD, "Systemic endothelial activation occurs in both mild and severe malaria. Correlating dermal microvascular endothelial cell phenotype and soluble cell adhesion molecules with disease severity", Am J Pathol, 152, pp.1477~1487 (1998)
- Pain A, "Platelet-mediated clumping of Plasmodium falciparum-infected erythrocytes is a common adhesive phenotype and is associated with severe malaria", Proc Natl Acad Sci USA, 98, pp.1805~1810 (2001)
- Netea MG, "Circulating cytokines as mediators of fever", Clin Infect Dis, 31(suppl), pp.178~184 (2000)
- Maitland K1, "falciparum malaria in Kenyan children : evidence for hypovolaemia", QJM, 96, pp.427~434 (2003)
- Perkins DJ, "Inverse relationship of plasma prostaglandin E2 and blood mononuclear cell cyclooxygenase-2 with disease severity in children with Plasmodium falciparum malaria", J Infect Dis, 183, pp.113~118 (2001)
- Schofield L, "Signal transduction in host cells by a glycosylphosphatidylinositol toxin of malaria parasites", J Exp Med, 177, pp.145~153 (1993)
- Olaniyan SA, "Tumour necrosis factor alpha promoter polymorphism, TNF-238 is associated with severe clinical outcome of falciparum malaria in Ibadan southwest Nigeria", Acta Trop, 161, pp.62~67 (2016)
- Clark IA, "The pathophysiology of falciparum malaria", Pharmacol Ther, 99, pp.221~260 (2003)
- Grau GE, "Tumor necrosis factor and disease severity in children with falciparum malaria", New Engl J Med, 320, pp.1586~1591 (1989)
- Kwiatkowski D, "TNF concentration in fatal cerebral, non-fatal cerebral, and uncomplicated Plasmodium falciparum malaria", Lancet, 336, pp.1201~1204 (1990)
- Perkins DJ, "Reduced interleukin-12and transforming growth factor—β1 in severe childhood malaria : relationship of cytokine balance with disease severity", J Infect Dis, 182, pp.988~992 (2000)
- Wenisch C, "Decreased serum levels of TGF-beta in patients with acute Plasmodium falciparum malaria", J Clin Immunol, 15, pp.69~73 (1995)
- Keswani T, "Role of TGF-β and IL-6 in dendritic cells, Treg and Th17 mediated immune response during experimental cerebral malaria", Cytokine, 88, pp.154~166 (2016)
