Cytopathogenicity of Entamoeba histolytica
The lesions induced in man by Entamoeba histolytica are characterized by massive tissue injury in the absence of major local signs of a host immune response. The amoeba damages surrounding cells preferentially by contact-mediated cytolysis. Recently, a presumptive aetiological factor underlying this...
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Veröffentlicht in: | Philosophical transactions of the Royal Society of London. Series B, Biological sciences Biological sciences, 1984-11, Vol.307 (1131), p.73-85 |
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description | The lesions induced in man by Entamoeba histolytica are characterized by massive tissue injury in the absence of major local signs of a host immune response. The amoeba damages surrounding cells preferentially by contact-mediated cytolysis. Recently, a presumptive aetiological factor underlying this process has been identified. It is a protein, amoebapore, capable of spontaneous incorporation into host cell membranes. Therein it induces high conductance ion-channels which rapidly collapse the cellular transmembrane potential and lead to a prelytic state. Amoebapore is present within the amoeba in a highly aggregated state in a small, dense particle. It is shed into the medium in a particulate form by a stimulus-mediated process. Release is enhanced by addition of concanavalin A, lipopolysaccharide or the calcium ionophore A23187. Surface-labelling of intact amoeba, followed by fractionation of the homogenate in self-generating Percoll gradients, identified two labelled fractions, the plasma membrane and a particulate fraction sedimenting in the region of intracellular particulate amoebapore. This latter fraction appears to be material in the process of exocytosis. A highly immunogenic surface lipid has been identified and shown to be involved in the rapid surface redistribution of immune complexes, their shedding and endocytosis. The relevance of these findings to the immunoprophylaxis of amoebiasis is discussed. |
doi_str_mv | 10.1098/rstb.1984.0110 |
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The amoeba damages surrounding cells preferentially by contact-mediated cytolysis. Recently, a presumptive aetiological factor underlying this process has been identified. It is a protein, amoebapore, capable of spontaneous incorporation into host cell membranes. Therein it induces high conductance ion-channels which rapidly collapse the cellular transmembrane potential and lead to a prelytic state. Amoebapore is present within the amoeba in a highly aggregated state in a small, dense particle. It is shed into the medium in a particulate form by a stimulus-mediated process. Release is enhanced by addition of concanavalin A, lipopolysaccharide or the calcium ionophore A23187. Surface-labelling of intact amoeba, followed by fractionation of the homogenate in self-generating Percoll gradients, identified two labelled fractions, the plasma membrane and a particulate fraction sedimenting in the region of intracellular particulate amoebapore. This latter fraction appears to be material in the process of exocytosis. A highly immunogenic surface lipid has been identified and shown to be involved in the rapid surface redistribution of immune complexes, their shedding and endocytosis. The relevance of these findings to the immunoprophylaxis of amoebiasis is discussed.</description><identifier>ISSN: 0962-8436</identifier><identifier>ISSN: 0080-4622</identifier><identifier>EISSN: 1471-2970</identifier><identifier>EISSN: 2054-0280</identifier><identifier>DOI: 10.1098/rstb.1984.0110</identifier><identifier>PMID: 6151690</identifier><identifier>CODEN: PTRBAE</identifier><language>eng</language><publisher>London: The Royal Society</publisher><subject>Amebiasis ; Amebiasis - parasitology ; Amibiasis ; Amoeba ; Animals ; Antibodies ; Antibody Formation ; Antigens, Protozoan - immunology ; Antiserum ; Biological and medical sciences ; Calcium ; Cell Membrane - immunology ; Cell membranes ; Cell Survival ; Cytolysis ; Entamoeba histolytica - immunology ; Entamoeba histolytica - pathogenicity ; Entamoebiasis - immunology ; Entamoebiasis - parasitology ; Host-Parasite Interactions ; Human protozoal diseases ; Humans ; Infectious diseases ; Lipids ; Medical sciences ; Membrane Lipids - immunology ; Membrane proteins ; Membrane Proteins - immunology ; Parasitic diseases ; Phagocytosis ; Protozoal diseases ; Trophozoites ; Tropical medicine</subject><ispartof>Philosophical transactions of the Royal Society of London. 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Series B, Biological sciences</title><addtitle>Phil. Trans. R. Soc. Lond. B</addtitle><addtitle>Philos Trans R Soc Lond B Biol Sci</addtitle><description>The lesions induced in man by Entamoeba histolytica are characterized by massive tissue injury in the absence of major local signs of a host immune response. The amoeba damages surrounding cells preferentially by contact-mediated cytolysis. Recently, a presumptive aetiological factor underlying this process has been identified. It is a protein, amoebapore, capable of spontaneous incorporation into host cell membranes. Therein it induces high conductance ion-channels which rapidly collapse the cellular transmembrane potential and lead to a prelytic state. Amoebapore is present within the amoeba in a highly aggregated state in a small, dense particle. It is shed into the medium in a particulate form by a stimulus-mediated process. Release is enhanced by addition of concanavalin A, lipopolysaccharide or the calcium ionophore A23187. Surface-labelling of intact amoeba, followed by fractionation of the homogenate in self-generating Percoll gradients, identified two labelled fractions, the plasma membrane and a particulate fraction sedimenting in the region of intracellular particulate amoebapore. This latter fraction appears to be material in the process of exocytosis. A highly immunogenic surface lipid has been identified and shown to be involved in the rapid surface redistribution of immune complexes, their shedding and endocytosis. The relevance of these findings to the immunoprophylaxis of amoebiasis is discussed.</description><subject>Amebiasis</subject><subject>Amebiasis - parasitology</subject><subject>Amibiasis</subject><subject>Amoeba</subject><subject>Animals</subject><subject>Antibodies</subject><subject>Antibody Formation</subject><subject>Antigens, Protozoan - immunology</subject><subject>Antiserum</subject><subject>Biological and medical sciences</subject><subject>Calcium</subject><subject>Cell Membrane - immunology</subject><subject>Cell membranes</subject><subject>Cell Survival</subject><subject>Cytolysis</subject><subject>Entamoeba histolytica - immunology</subject><subject>Entamoeba histolytica - pathogenicity</subject><subject>Entamoebiasis - immunology</subject><subject>Entamoebiasis - parasitology</subject><subject>Host-Parasite Interactions</subject><subject>Human protozoal diseases</subject><subject>Humans</subject><subject>Infectious diseases</subject><subject>Lipids</subject><subject>Medical sciences</subject><subject>Membrane Lipids - immunology</subject><subject>Membrane proteins</subject><subject>Membrane Proteins - immunology</subject><subject>Parasitic diseases</subject><subject>Phagocytosis</subject><subject>Protozoal diseases</subject><subject>Trophozoites</subject><subject>Tropical medicine</subject><issn>0962-8436</issn><issn>0080-4622</issn><issn>1471-2970</issn><issn>2054-0280</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1984</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kc-L1DAUx4Mo6zh69aQwB_EgdDavaZrksuAO6w9YEHTuIc2kOxk6TU1SpfvXm7bD4CLuKQnv877f975B6DXgNWDBL32I1RoEL9YYAD9BCygYZLlg-ClaYFHmGS9I-Ry9COGAMRaUFRfoogQKpcAL9GEzRNepuHd3prXaxmHl6tVNG9XRmUqt9jZE1wzRavUSPatVE8yr07lE2083282X7Pbb56-bj7eZppzFrCpJwStGFQEuClIpAL2japcDpbkAxbimVZ3uRlCMK5ansRNVGVUQKiqyRO9n2c67n70JUR5t0KZpVGtcHySjaSGekwSuZ1B7F4I3tey8PSo_SMByzEaO2cgxGzlmkxrenpT76mh2Z_wURqq_O9VV0KqpvWq1DWdMQM7KZLxEZMa8G1IOTlsTB3lwvW_T8__m4bGu7z-21yBK8YtgZgEISMwJYFpwguW97Sa5EZAJkDaE3sgJe2jzr-ub2fWQvtGfV8mFwEDLVL6ay3t7t_9tvZEPppvEtGujaePkOzkyIuu-aWS3q5PA5aMCbuiSxF-t5A_eJtJw</recordid><startdate>19841113</startdate><enddate>19841113</enddate><creator>Gitler, C.</creator><creator>Calef, Edna</creator><creator>Rosenberg, I.</creator><general>The Royal Society</general><general>Royal Society of London</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>19841113</creationdate><title>Cytopathogenicity of Entamoeba histolytica</title><author>Gitler, C. ; Calef, Edna ; Rosenberg, I.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c587t-b6348b75a318943ba11cd5ad2155291a78c5bf552e9500b721103babea4359b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1984</creationdate><topic>Amebiasis</topic><topic>Amebiasis - parasitology</topic><topic>Amibiasis</topic><topic>Amoeba</topic><topic>Animals</topic><topic>Antibodies</topic><topic>Antibody Formation</topic><topic>Antigens, Protozoan - immunology</topic><topic>Antiserum</topic><topic>Biological and medical sciences</topic><topic>Calcium</topic><topic>Cell Membrane - immunology</topic><topic>Cell membranes</topic><topic>Cell Survival</topic><topic>Cytolysis</topic><topic>Entamoeba histolytica - immunology</topic><topic>Entamoeba histolytica - pathogenicity</topic><topic>Entamoebiasis - immunology</topic><topic>Entamoebiasis - parasitology</topic><topic>Host-Parasite Interactions</topic><topic>Human protozoal diseases</topic><topic>Humans</topic><topic>Infectious diseases</topic><topic>Lipids</topic><topic>Medical sciences</topic><topic>Membrane Lipids - immunology</topic><topic>Membrane proteins</topic><topic>Membrane Proteins - immunology</topic><topic>Parasitic diseases</topic><topic>Phagocytosis</topic><topic>Protozoal diseases</topic><topic>Trophozoites</topic><topic>Tropical medicine</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gitler, C.</creatorcontrib><creatorcontrib>Calef, Edna</creatorcontrib><creatorcontrib>Rosenberg, I.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Philosophical transactions of the Royal Society of London. Series B, Biological sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gitler, C.</au><au>Calef, Edna</au><au>Rosenberg, I.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cytopathogenicity of Entamoeba histolytica</atitle><jtitle>Philosophical transactions of the Royal Society of London. Series B, Biological sciences</jtitle><stitle>Phil. Trans. R. Soc. Lond. B</stitle><addtitle>Philos Trans R Soc Lond B Biol Sci</addtitle><date>1984-11-13</date><risdate>1984</risdate><volume>307</volume><issue>1131</issue><spage>73</spage><epage>85</epage><pages>73-85</pages><issn>0962-8436</issn><issn>0080-4622</issn><eissn>1471-2970</eissn><eissn>2054-0280</eissn><coden>PTRBAE</coden><abstract>The lesions induced in man by Entamoeba histolytica are characterized by massive tissue injury in the absence of major local signs of a host immune response. The amoeba damages surrounding cells preferentially by contact-mediated cytolysis. Recently, a presumptive aetiological factor underlying this process has been identified. It is a protein, amoebapore, capable of spontaneous incorporation into host cell membranes. Therein it induces high conductance ion-channels which rapidly collapse the cellular transmembrane potential and lead to a prelytic state. Amoebapore is present within the amoeba in a highly aggregated state in a small, dense particle. It is shed into the medium in a particulate form by a stimulus-mediated process. Release is enhanced by addition of concanavalin A, lipopolysaccharide or the calcium ionophore A23187. Surface-labelling of intact amoeba, followed by fractionation of the homogenate in self-generating Percoll gradients, identified two labelled fractions, the plasma membrane and a particulate fraction sedimenting in the region of intracellular particulate amoebapore. This latter fraction appears to be material in the process of exocytosis. A highly immunogenic surface lipid has been identified and shown to be involved in the rapid surface redistribution of immune complexes, their shedding and endocytosis. The relevance of these findings to the immunoprophylaxis of amoebiasis is discussed.</abstract><cop>London</cop><pub>The Royal Society</pub><pmid>6151690</pmid><doi>10.1098/rstb.1984.0110</doi><tpages>13</tpages></addata></record> |
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subjects | Amebiasis Amebiasis - parasitology Amibiasis Amoeba Animals Antibodies Antibody Formation Antigens, Protozoan - immunology Antiserum Biological and medical sciences Calcium Cell Membrane - immunology Cell membranes Cell Survival Cytolysis Entamoeba histolytica - immunology Entamoeba histolytica - pathogenicity Entamoebiasis - immunology Entamoebiasis - parasitology Host-Parasite Interactions Human protozoal diseases Humans Infectious diseases Lipids Medical sciences Membrane Lipids - immunology Membrane proteins Membrane Proteins - immunology Parasitic diseases Phagocytosis Protozoal diseases Trophozoites Tropical medicine |
title | Cytopathogenicity of Entamoeba histolytica |
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