INHIBITION OF TRYPANOSOMA CRUZI EGRESS FROM INFECTED FIBROBLASTS IS MEDIATED BY CD4+ AND μ+ IMMUNE CELLS
Trypanosoma cruzi, the causative agent of Chagas disease, is able to reproduce intracellularly in many host cell types while in the mammalian host. Although cellular immunity is known to be important in resistance to infection, the ability of immune cells to interfere with the completion of the intr...
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| Veröffentlicht in: | The Journal of parasitology 2003-08, Vol.89 (4), p.733-737, Article 733 |
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| description | Trypanosoma cruzi, the causative agent of Chagas disease, is able to reproduce intracellularly in many host cell types while in the mammalian host. Although cellular immunity is known to be important in resistance to infection, the ability of immune cells to interfere with the completion of the intracellular growth cycle of T. cruzi has not been described. Using a tissue culture system to study the parasite growth cycle, we have found that spleen cells from infected mice are able to decrease the number of parasites released from infected fibroblasts. Spleen cells from mice infected for as few as 14 days and as long as 300 days display this inhibitory ability. Parasite egress from infected cells is inhibited by factor(s) released by immune cells during coculture with infected fibroblasts. Immune cell depletion studies indicate that the inhibitory activity requires the presence of both CD4+ T cells and μ+ B cells. These results suggest a direct ability of immune cells to somehow interfere with the completion of the intracellular cycle, and this ability may play a role in control of this parasite. |
| doi_str_mv | 10.1645/GE-77R |
| format | Article |
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Although cellular immunity is known to be important in resistance to infection, the ability of immune cells to interfere with the completion of the intracellular growth cycle of T. cruzi has not been described. Using a tissue culture system to study the parasite growth cycle, we have found that spleen cells from infected mice are able to decrease the number of parasites released from infected fibroblasts. Spleen cells from mice infected for as few as 14 days and as long as 300 days display this inhibitory ability. Parasite egress from infected cells is inhibited by factor(s) released by immune cells during coculture with infected fibroblasts. Immune cell depletion studies indicate that the inhibitory activity requires the presence of both CD4+ T cells and μ+ B cells. These results suggest a direct ability of immune cells to somehow interfere with the completion of the intracellular cycle, and this ability may play a role in control of this parasite.</description><identifier>ISSN: 0022-3395</identifier><identifier>EISSN: 1937-2345</identifier><identifier>DOI: 10.1645/GE-77R</identifier><identifier>PMID: 14533683</identifier><identifier>CODEN: JOPAA2</identifier><language>eng</language><publisher>Lawrence, KS: American Society of Parasitologists</publisher><subject>Animals ; B lymphocytes ; B-Lymphocytes - immunology ; Biological and medical sciences ; CD4 antigen ; CD4-Positive T-Lymphocytes - immunology ; Cell culture ; Cell Line ; Cell Separation ; Cell-mediated immunity ; Chagas disease ; Chagas Disease - immunology ; Chagas Disease - parasitology ; Coculture Techniques ; Cultured cells ; Depletion ; Egress ; Experimental helminthic diseases. Models ; Female ; Fibroblasts ; Fibroblasts - parasitology ; Helminthic diseases ; Immune system ; Immunity, Cellular ; IMMUNOLOGY ; Infections ; Infectious diseases ; Intracellular ; Lymphocytes ; Lymphocytes B ; Lymphocytes T ; Medical sciences ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C3H ; Parasite hosts ; Parasites ; Parasitic diseases ; Spleen ; Spleen - cytology ; Spleen - immunology ; Spleen cells ; T lymphocytes ; Tissue culture ; Trypanosoma cruzi - immunology ; Vector-borne diseases</subject><ispartof>The Journal of parasitology, 2003-08, Vol.89 (4), p.733-737, Article 733</ispartof><rights>American Society of Parasitologists</rights><rights>Copyright 2003 American Society of Parasitologists</rights><rights>2004 INIST-CNRS</rights><rights>Copyright Allen Press Inc. Aug 2003</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b383t-9210acec81378658aff54dd1e9f88bf3300b4994b595b837292512656761542f3</citedby><cites>FETCH-LOGICAL-b383t-9210acec81378658aff54dd1e9f88bf3300b4994b595b837292512656761542f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://bioone.org/doi/pdf/10.1645/GE-77R$$EPDF$$P50$$Gbioone$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/3285869$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>314,780,784,803,26969,27915,27916,52354,58008,58241</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15162849$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14533683$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rowland, Edwin C</creatorcontrib><creatorcontrib>Chen, Zhuo</creatorcontrib><title>INHIBITION OF TRYPANOSOMA CRUZI EGRESS FROM INFECTED FIBROBLASTS IS MEDIATED BY CD4+ AND μ+ IMMUNE CELLS</title><title>The Journal of parasitology</title><addtitle>J Parasitol</addtitle><description>Trypanosoma cruzi, the causative agent of Chagas disease, is able to reproduce intracellularly in many host cell types while in the mammalian host. Although cellular immunity is known to be important in resistance to infection, the ability of immune cells to interfere with the completion of the intracellular growth cycle of T. cruzi has not been described. Using a tissue culture system to study the parasite growth cycle, we have found that spleen cells from infected mice are able to decrease the number of parasites released from infected fibroblasts. Spleen cells from mice infected for as few as 14 days and as long as 300 days display this inhibitory ability. Parasite egress from infected cells is inhibited by factor(s) released by immune cells during coculture with infected fibroblasts. Immune cell depletion studies indicate that the inhibitory activity requires the presence of both CD4+ T cells and μ+ B cells. These results suggest a direct ability of immune cells to somehow interfere with the completion of the intracellular cycle, and this ability may play a role in control of this parasite.</description><subject>Animals</subject><subject>B lymphocytes</subject><subject>B-Lymphocytes - immunology</subject><subject>Biological and medical sciences</subject><subject>CD4 antigen</subject><subject>CD4-Positive T-Lymphocytes - immunology</subject><subject>Cell culture</subject><subject>Cell Line</subject><subject>Cell Separation</subject><subject>Cell-mediated immunity</subject><subject>Chagas disease</subject><subject>Chagas Disease - immunology</subject><subject>Chagas Disease - parasitology</subject><subject>Coculture Techniques</subject><subject>Cultured cells</subject><subject>Depletion</subject><subject>Egress</subject><subject>Experimental helminthic diseases. Models</subject><subject>Female</subject><subject>Fibroblasts</subject><subject>Fibroblasts - parasitology</subject><subject>Helminthic diseases</subject><subject>Immune system</subject><subject>Immunity, Cellular</subject><subject>IMMUNOLOGY</subject><subject>Infections</subject><subject>Infectious diseases</subject><subject>Intracellular</subject><subject>Lymphocytes</subject><subject>Lymphocytes B</subject><subject>Lymphocytes T</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Inbred C3H</subject><subject>Parasite hosts</subject><subject>Parasites</subject><subject>Parasitic diseases</subject><subject>Spleen</subject><subject>Spleen - cytology</subject><subject>Spleen - immunology</subject><subject>Spleen cells</subject><subject>T lymphocytes</subject><subject>Tissue culture</subject><subject>Trypanosoma cruzi - immunology</subject><subject>Vector-borne diseases</subject><issn>0022-3395</issn><issn>1937-2345</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp1kN2K00AYhgdR3LrqFYgMrOvJGp2fTDJzmKaT7kB-JEkP1pMwSRNISZM1kx54b3sNXpMpLRZWPPgY-Obh-V5eAN5j9BU7Nvu2lpbrpi_AAgvqWoTa7CVYIESIRalgV-CNMTuEEJvnNbjCNqPU4XQBWhXfq6XKVRLDJIB5-vDdi5MsiTzop5sfCsp1KrMMBmkSQRUH0s_lCgZqmSbL0MvyDKoMRnKlvON--QD9lX0HvXgFfz_dQRVFm1hCX4Zh9ha8anRn6nfn9xpsApn791aYrJXvhVZJOZ0sQTDSVV1xTF3uMK6bhtnbLa5Fw3nZUIpQaQthl0ywklOXCMIwcZjjOpjZpKHX4PPJ-zgOPw-1mYp9a6q663RfDwdTuMx1KHbFDN48A3fDYeznbMXsY4hiRvhFV42DMWPdFI9ju9fjrwKj4lh9sZbFXP0MfjzrDuW-3l6wc9czcHsGtKl014y6r1pz4Rh2CLePub48u1i1k57aoZ9G3Xb_3v1wwndmGsa_Oko4487R9un0XbbD0Nf_S_8Hbo6juA</recordid><startdate>20030801</startdate><enddate>20030801</enddate><creator>Rowland, Edwin C</creator><creator>Chen, Zhuo</creator><general>American Society of Parasitologists</general><general>Allen Press Inc</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>3V.</scope><scope>7QG</scope><scope>7SN</scope><scope>7SS</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20030801</creationdate><title>INHIBITION OF TRYPANOSOMA CRUZI EGRESS FROM INFECTED FIBROBLASTS IS MEDIATED BY CD4+ AND μ+ IMMUNE CELLS</title><author>Rowland, Edwin C ; Chen, Zhuo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b383t-9210acec81378658aff54dd1e9f88bf3300b4994b595b837292512656761542f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Animals</topic><topic>B lymphocytes</topic><topic>B-Lymphocytes - immunology</topic><topic>Biological and medical sciences</topic><topic>CD4 antigen</topic><topic>CD4-Positive T-Lymphocytes - immunology</topic><topic>Cell culture</topic><topic>Cell Line</topic><topic>Cell Separation</topic><topic>Cell-mediated immunity</topic><topic>Chagas disease</topic><topic>Chagas Disease - immunology</topic><topic>Chagas Disease - parasitology</topic><topic>Coculture Techniques</topic><topic>Cultured cells</topic><topic>Depletion</topic><topic>Egress</topic><topic>Experimental helminthic diseases. Models</topic><topic>Female</topic><topic>Fibroblasts</topic><topic>Fibroblasts - parasitology</topic><topic>Helminthic diseases</topic><topic>Immune system</topic><topic>Immunity, Cellular</topic><topic>IMMUNOLOGY</topic><topic>Infections</topic><topic>Infectious diseases</topic><topic>Intracellular</topic><topic>Lymphocytes</topic><topic>Lymphocytes B</topic><topic>Lymphocytes T</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Inbred C3H</topic><topic>Parasite hosts</topic><topic>Parasites</topic><topic>Parasitic diseases</topic><topic>Spleen</topic><topic>Spleen - cytology</topic><topic>Spleen - immunology</topic><topic>Spleen cells</topic><topic>T lymphocytes</topic><topic>Tissue culture</topic><topic>Trypanosoma cruzi - immunology</topic><topic>Vector-borne diseases</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rowland, Edwin C</creatorcontrib><creatorcontrib>Chen, Zhuo</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>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>ProQuest Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection (Proquest) (PQ_SDU_P3)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biological Sciences</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>The Journal of parasitology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Rowland, Edwin C</au><au>Chen, Zhuo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>INHIBITION OF TRYPANOSOMA CRUZI EGRESS FROM INFECTED FIBROBLASTS IS MEDIATED BY CD4+ AND μ+ IMMUNE CELLS</atitle><jtitle>The Journal of parasitology</jtitle><addtitle>J Parasitol</addtitle><date>2003-08-01</date><risdate>2003</risdate><volume>89</volume><issue>4</issue><spage>733</spage><epage>737</epage><pages>733-737</pages><artnum>733</artnum><issn>0022-3395</issn><eissn>1937-2345</eissn><coden>JOPAA2</coden><abstract>Trypanosoma cruzi, the causative agent of Chagas disease, is able to reproduce intracellularly in many host cell types while in the mammalian host. Although cellular immunity is known to be important in resistance to infection, the ability of immune cells to interfere with the completion of the intracellular growth cycle of T. cruzi has not been described. Using a tissue culture system to study the parasite growth cycle, we have found that spleen cells from infected mice are able to decrease the number of parasites released from infected fibroblasts. Spleen cells from mice infected for as few as 14 days and as long as 300 days display this inhibitory ability. Parasite egress from infected cells is inhibited by factor(s) released by immune cells during coculture with infected fibroblasts. Immune cell depletion studies indicate that the inhibitory activity requires the presence of both CD4+ T cells and μ+ B cells. These results suggest a direct ability of immune cells to somehow interfere with the completion of the intracellular cycle, and this ability may play a role in control of this parasite.</abstract><cop>Lawrence, KS</cop><pub>American Society of Parasitologists</pub><pmid>14533683</pmid><doi>10.1645/GE-77R</doi><tpages>5</tpages></addata></record> |
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| ispartof | The Journal of parasitology, 2003-08, Vol.89 (4), p.733-737, Article 733 |
| issn | 0022-3395 1937-2345 |
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| subjects | Animals B lymphocytes B-Lymphocytes - immunology Biological and medical sciences CD4 antigen CD4-Positive T-Lymphocytes - immunology Cell culture Cell Line Cell Separation Cell-mediated immunity Chagas disease Chagas Disease - immunology Chagas Disease - parasitology Coculture Techniques Cultured cells Depletion Egress Experimental helminthic diseases. Models Female Fibroblasts Fibroblasts - parasitology Helminthic diseases Immune system Immunity, Cellular IMMUNOLOGY Infections Infectious diseases Intracellular Lymphocytes Lymphocytes B Lymphocytes T Medical sciences Mice Mice, Inbred BALB C Mice, Inbred C3H Parasite hosts Parasites Parasitic diseases Spleen Spleen - cytology Spleen - immunology Spleen cells T lymphocytes Tissue culture Trypanosoma cruzi - immunology Vector-borne diseases |
| title | INHIBITION OF TRYPANOSOMA CRUZI EGRESS FROM INFECTED FIBROBLASTS IS MEDIATED BY CD4+ AND μ+ IMMUNE CELLS |
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