Entamoeba histolytica: Lymphoreticular Changes in Gerbils (Meriones unguiculatus) with Experimentally Induced Cecal Amebiasis
Antibody responses and changes in the lymphoreticular tissues of gerbils with experimental cecal amebiasis were studied from 5 to 60 days PI. Changes in the cecum consisted of lymphoid follicle hyperplasia and depletion of lymphocytes, followed by follicle atrophy and histiocytosis. Mesenteric lymph...
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Veröffentlicht in: | The Journal of parasitology 1985-10, Vol.71 (5), p.566-575 |
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description | Antibody responses and changes in the lymphoreticular tissues of gerbils with experimental cecal amebiasis were studied from 5 to 60 days PI. Changes in the cecum consisted of lymphoid follicle hyperplasia and depletion of lymphocytes, followed by follicle atrophy and histiocytosis. Mesenteric lymphadenopathy, and histologic alterations in the lymph nodes paralleled the progressive development of amebic cecal lesions. Early in the infection (5 to 10 days PI) mesenteric lymph nodes showed cortical follicle hyperplasia, blastogenesis in the paracortical areas (PCA) and intense lymphoblast and plasma cell activity in the medullary cords. At 20 to 30 days PI, the cortical follicles, the PCA and the medulla were depleted of lymphocytes and there was histiocytosis throughout the organ. At 60 days PI, lymphocyte repopulation took place in the PCA, and cortical follicles had active germinal centers. Spleen follicles did not increase in number as the infection progressed, but became hyperplastic. Antibody titers to ameba were low throughout the cecal infection but rose whenever amebic metastasis to the liver occurred. The results of this study indicate that lymphocytes from the submucosal lymphoid follicles and the draining lymph nodes may control the pathogenesis of the infection. Lymphoreticular tissue alterations could result from antigenic stimulation and migration of cells to the sites of infection. |
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Changes in the cecum consisted of lymphoid follicle hyperplasia and depletion of lymphocytes, followed by follicle atrophy and histiocytosis. Mesenteric lymphadenopathy, and histologic alterations in the lymph nodes paralleled the progressive development of amebic cecal lesions. Early in the infection (5 to 10 days PI) mesenteric lymph nodes showed cortical follicle hyperplasia, blastogenesis in the paracortical areas (PCA) and intense lymphoblast and plasma cell activity in the medullary cords. At 20 to 30 days PI, the cortical follicles, the PCA and the medulla were depleted of lymphocytes and there was histiocytosis throughout the organ. At 60 days PI, lymphocyte repopulation took place in the PCA, and cortical follicles had active germinal centers. Spleen follicles did not increase in number as the infection progressed, but became hyperplastic. Antibody titers to ameba were low throughout the cecal infection but rose whenever amebic metastasis to the liver occurred. The results of this study indicate that lymphocytes from the submucosal lymphoid follicles and the draining lymph nodes may control the pathogenesis of the infection. Lymphoreticular tissue alterations could result from antigenic stimulation and migration of cells to the sites of infection.</description><identifier>ISSN: 0022-3395</identifier><identifier>EISSN: 1937-2345</identifier><identifier>DOI: 10.2307/3281425</identifier><identifier>PMID: 2865345</identifier><identifier>CODEN: JOPAA2</identifier><language>eng</language><publisher>Lawrence, KS: American Society of Parasitologists</publisher><subject>Amebiasis ; Amibiasis ; Animals ; Antibodies - analysis ; Biological and medical sciences ; Cecal Diseases - immunology ; Cecal Diseases - pathology ; Cecum - pathology ; Dysentery, Amebic - immunology ; Dysentery, Amebic - pathology ; Entamoeba histolytica - immunology ; Experimental protozoal diseases and models ; Follicles ; Gerbillinae ; Histiocytes - pathology ; Histology ; Human protozoal diseases ; Infections ; Infectious diseases ; Intestinal Mucosa - pathology ; Lesions ; Liver Abscess, Amebic - immunology ; Liver Abscess, Amebic - pathology ; Lymph nodes ; Lymph Nodes - immunology ; Lymph Nodes - pathology ; Lymphocytes ; Lymphocytes - immunology ; Lymphocytes - pathology ; Lymphoid tissue ; Lymphoid Tissue - immunology ; Lymphoid Tissue - pathology ; Male ; Medical sciences ; Memory interference ; Organ Size ; Parasitic diseases ; Pathology ; Plasma Cells - pathology ; Protozoal diseases ; Spleen ; Spleen - immunology ; Spleen - pathology ; Splenomegaly ; Tropical medicine</subject><ispartof>The Journal of parasitology, 1985-10, Vol.71 (5), p.566-575</ispartof><rights>Copyright 1985 American Society of Parasitologists</rights><rights>1986 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c334t-8b29daa5866ff43592a7f97289b47770ecddfa284e3086fd9cb366af46ba5cb3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/3281425$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/3281425$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>314,780,784,803,27924,27925,58017,58250</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=8517575$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/2865345$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chadee, K.</creatorcontrib><creatorcontrib>Meerovitch, E.</creatorcontrib><title>Entamoeba histolytica: Lymphoreticular Changes in Gerbils (Meriones unguiculatus) with Experimentally Induced Cecal Amebiasis</title><title>The Journal of parasitology</title><addtitle>J Parasitol</addtitle><description>Antibody responses and changes in the lymphoreticular tissues of gerbils with experimental cecal amebiasis were studied from 5 to 60 days PI. Changes in the cecum consisted of lymphoid follicle hyperplasia and depletion of lymphocytes, followed by follicle atrophy and histiocytosis. Mesenteric lymphadenopathy, and histologic alterations in the lymph nodes paralleled the progressive development of amebic cecal lesions. Early in the infection (5 to 10 days PI) mesenteric lymph nodes showed cortical follicle hyperplasia, blastogenesis in the paracortical areas (PCA) and intense lymphoblast and plasma cell activity in the medullary cords. At 20 to 30 days PI, the cortical follicles, the PCA and the medulla were depleted of lymphocytes and there was histiocytosis throughout the organ. At 60 days PI, lymphocyte repopulation took place in the PCA, and cortical follicles had active germinal centers. Spleen follicles did not increase in number as the infection progressed, but became hyperplastic. Antibody titers to ameba were low throughout the cecal infection but rose whenever amebic metastasis to the liver occurred. The results of this study indicate that lymphocytes from the submucosal lymphoid follicles and the draining lymph nodes may control the pathogenesis of the infection. Lymphoreticular tissue alterations could result from antigenic stimulation and migration of cells to the sites of infection.</description><subject>Amebiasis</subject><subject>Amibiasis</subject><subject>Animals</subject><subject>Antibodies - analysis</subject><subject>Biological and medical sciences</subject><subject>Cecal Diseases - immunology</subject><subject>Cecal Diseases - pathology</subject><subject>Cecum - pathology</subject><subject>Dysentery, Amebic - immunology</subject><subject>Dysentery, Amebic - pathology</subject><subject>Entamoeba histolytica - immunology</subject><subject>Experimental protozoal diseases and models</subject><subject>Follicles</subject><subject>Gerbillinae</subject><subject>Histiocytes - pathology</subject><subject>Histology</subject><subject>Human protozoal diseases</subject><subject>Infections</subject><subject>Infectious diseases</subject><subject>Intestinal Mucosa - pathology</subject><subject>Lesions</subject><subject>Liver Abscess, Amebic - immunology</subject><subject>Liver Abscess, Amebic - pathology</subject><subject>Lymph nodes</subject><subject>Lymph Nodes - immunology</subject><subject>Lymph Nodes - pathology</subject><subject>Lymphocytes</subject><subject>Lymphocytes - immunology</subject><subject>Lymphocytes - pathology</subject><subject>Lymphoid tissue</subject><subject>Lymphoid Tissue - immunology</subject><subject>Lymphoid Tissue - pathology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Memory interference</subject><subject>Organ Size</subject><subject>Parasitic diseases</subject><subject>Pathology</subject><subject>Plasma Cells - pathology</subject><subject>Protozoal diseases</subject><subject>Spleen</subject><subject>Spleen - immunology</subject><subject>Spleen - pathology</subject><subject>Splenomegaly</subject><subject>Tropical medicine</subject><issn>0022-3395</issn><issn>1937-2345</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1985</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kEtr3DAUhUVJSCdp6S8oaBHaZuFW1sOyswvD5AETupm9uZavMgqyPZVskln0v1fJmNBNFkK6Oh_ncg4hX3L2kwumfwle5pKrD2SRV0JnXEh1RBaMcZ4JUamP5DTGR8aYSueEnPCyUAlZkL-rfoRuwAbo1sVx8PvRGbik63232w4B0zR5CHS5hf4BI3U9vcHQOB_pj3sMbujT59Q_TK_cOMUL-uTGLV0975LaYXL3fk_v-nYy2NIlGvD0qsPGQXTxEzm24CN-nu8zsrlebZa32fr3zd3yap0ZIeSYlQ2vWgBVFoW1UqiKg7aV5mXVSK01Q9O2FngpUbCysG1lGlEUYGXRgErvM_LtYLsLw58J41h3Lhr0HnocpljrQgrNpE7g9wNowhBjQFvvUggI-zpn9UvP9dxzIr_OllPTYfvGzcUm_XzWIabINkBvXHzDSpVrpf_DHlP34d1t_wCRXpGf</recordid><startdate>198510</startdate><enddate>198510</enddate><creator>Chadee, K.</creator><creator>Meerovitch, E.</creator><general>American Society of Parasitologists</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>198510</creationdate><title>Entamoeba histolytica: Lymphoreticular Changes in Gerbils (Meriones unguiculatus) with Experimentally Induced Cecal Amebiasis</title><author>Chadee, K. ; Meerovitch, E.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c334t-8b29daa5866ff43592a7f97289b47770ecddfa284e3086fd9cb366af46ba5cb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1985</creationdate><topic>Amebiasis</topic><topic>Amibiasis</topic><topic>Animals</topic><topic>Antibodies - analysis</topic><topic>Biological and medical sciences</topic><topic>Cecal Diseases - immunology</topic><topic>Cecal Diseases - pathology</topic><topic>Cecum - pathology</topic><topic>Dysentery, Amebic - immunology</topic><topic>Dysentery, Amebic - pathology</topic><topic>Entamoeba histolytica - immunology</topic><topic>Experimental protozoal diseases and models</topic><topic>Follicles</topic><topic>Gerbillinae</topic><topic>Histiocytes - pathology</topic><topic>Histology</topic><topic>Human protozoal diseases</topic><topic>Infections</topic><topic>Infectious diseases</topic><topic>Intestinal Mucosa - pathology</topic><topic>Lesions</topic><topic>Liver Abscess, Amebic - immunology</topic><topic>Liver Abscess, Amebic - pathology</topic><topic>Lymph nodes</topic><topic>Lymph Nodes - immunology</topic><topic>Lymph Nodes - pathology</topic><topic>Lymphocytes</topic><topic>Lymphocytes - immunology</topic><topic>Lymphocytes - pathology</topic><topic>Lymphoid tissue</topic><topic>Lymphoid Tissue - immunology</topic><topic>Lymphoid Tissue - pathology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Memory interference</topic><topic>Organ Size</topic><topic>Parasitic diseases</topic><topic>Pathology</topic><topic>Plasma Cells - pathology</topic><topic>Protozoal diseases</topic><topic>Spleen</topic><topic>Spleen - immunology</topic><topic>Spleen - pathology</topic><topic>Splenomegaly</topic><topic>Tropical medicine</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chadee, K.</creatorcontrib><creatorcontrib>Meerovitch, E.</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>The Journal of parasitology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chadee, K.</au><au>Meerovitch, E.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Entamoeba histolytica: Lymphoreticular Changes in Gerbils (Meriones unguiculatus) with Experimentally Induced Cecal Amebiasis</atitle><jtitle>The Journal of parasitology</jtitle><addtitle>J Parasitol</addtitle><date>1985-10</date><risdate>1985</risdate><volume>71</volume><issue>5</issue><spage>566</spage><epage>575</epage><pages>566-575</pages><issn>0022-3395</issn><eissn>1937-2345</eissn><coden>JOPAA2</coden><abstract>Antibody responses and changes in the lymphoreticular tissues of gerbils with experimental cecal amebiasis were studied from 5 to 60 days PI. Changes in the cecum consisted of lymphoid follicle hyperplasia and depletion of lymphocytes, followed by follicle atrophy and histiocytosis. Mesenteric lymphadenopathy, and histologic alterations in the lymph nodes paralleled the progressive development of amebic cecal lesions. Early in the infection (5 to 10 days PI) mesenteric lymph nodes showed cortical follicle hyperplasia, blastogenesis in the paracortical areas (PCA) and intense lymphoblast and plasma cell activity in the medullary cords. At 20 to 30 days PI, the cortical follicles, the PCA and the medulla were depleted of lymphocytes and there was histiocytosis throughout the organ. At 60 days PI, lymphocyte repopulation took place in the PCA, and cortical follicles had active germinal centers. Spleen follicles did not increase in number as the infection progressed, but became hyperplastic. Antibody titers to ameba were low throughout the cecal infection but rose whenever amebic metastasis to the liver occurred. The results of this study indicate that lymphocytes from the submucosal lymphoid follicles and the draining lymph nodes may control the pathogenesis of the infection. Lymphoreticular tissue alterations could result from antigenic stimulation and migration of cells to the sites of infection.</abstract><cop>Lawrence, KS</cop><pub>American Society of Parasitologists</pub><pmid>2865345</pmid><doi>10.2307/3281425</doi><tpages>10</tpages></addata></record> |
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subjects | Amebiasis Amibiasis Animals Antibodies - analysis Biological and medical sciences Cecal Diseases - immunology Cecal Diseases - pathology Cecum - pathology Dysentery, Amebic - immunology Dysentery, Amebic - pathology Entamoeba histolytica - immunology Experimental protozoal diseases and models Follicles Gerbillinae Histiocytes - pathology Histology Human protozoal diseases Infections Infectious diseases Intestinal Mucosa - pathology Lesions Liver Abscess, Amebic - immunology Liver Abscess, Amebic - pathology Lymph nodes Lymph Nodes - immunology Lymph Nodes - pathology Lymphocytes Lymphocytes - immunology Lymphocytes - pathology Lymphoid tissue Lymphoid Tissue - immunology Lymphoid Tissue - pathology Male Medical sciences Memory interference Organ Size Parasitic diseases Pathology Plasma Cells - pathology Protozoal diseases Spleen Spleen - immunology Spleen - pathology Splenomegaly Tropical medicine |
title | Entamoeba histolytica: Lymphoreticular Changes in Gerbils (Meriones unguiculatus) with Experimentally Induced Cecal Amebiasis |
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