Uptake of apoptotic cells drives the growth of a pathogenic trypanosome in macrophages
After apoptosis, phagocytes prevent inflammation and tissue damage by the uptake and removal of dead cells 1 . In addition, apoptotic cells evoke an anti-inflammatory response through macrophages 2 , 3 . We have previously shown that there is intense lymphocyte apoptosis in an experimental model of...
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| Veröffentlicht in: | Nature (London) 2000-01, Vol.403 (6766), p.199-203 |
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| creator | Freire-de-Lima, Célio G. Nascimento, Danielle O. Soares, Milena B. P. Bozza, Patricia T. Castro-Faria-Neto, Hugo C. de Mello, Fernando G. DosReis, George A. Lopes, Marcela F. |
| description | After apoptosis, phagocytes prevent inflammation and tissue damage by the uptake and removal of dead cells
1
. In addition, apoptotic cells evoke an anti-inflammatory response through macrophages
2
,
3
. We have previously shown that there is intense lymphocyte apoptosis in an experimental model of Chagas' disease
4
, a debilitating cardiac illness caused by the protozoan
Trypanosoma cruzi
. Here we show that the interaction of apoptotic, but not necrotic T lymphocytes with macrophages infected with
T. cruzi
fuels parasite growth in a manner dependent on prostaglandins, transforming growth factor-β (TGF-β) and polyamine biosynthesis. We show that the vitronectin receptor is critical, in both apoptotic-cell cytoadherence and the induction of prostaglandin E
2
/TGF-β release and ornithine decarboxylase activity in macrophages. A single injection of apoptotic cells in infected mice increases parasitaemia, whereas treatment with cyclooxygenase inhibitors almost completely ablates it
in vivo
. These results suggest that continual lymphocyte apoptosis and phagocytosis of apoptotic cells by macrophages have a role in parasite persistence in the host, and that cyclooxygenase inhibitors have potential therapeutic application in the control of parasite replication and spread in Chagas' disease. |
| doi_str_mv | 10.1038/35003208 |
| format | Article |
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1
. In addition, apoptotic cells evoke an anti-inflammatory response through macrophages
2
,
3
. We have previously shown that there is intense lymphocyte apoptosis in an experimental model of Chagas' disease
4
, a debilitating cardiac illness caused by the protozoan
Trypanosoma cruzi
. Here we show that the interaction of apoptotic, but not necrotic T lymphocytes with macrophages infected with
T. cruzi
fuels parasite growth in a manner dependent on prostaglandins, transforming growth factor-β (TGF-β) and polyamine biosynthesis. We show that the vitronectin receptor is critical, in both apoptotic-cell cytoadherence and the induction of prostaglandin E
2
/TGF-β release and ornithine decarboxylase activity in macrophages. A single injection of apoptotic cells in infected mice increases parasitaemia, whereas treatment with cyclooxygenase inhibitors almost completely ablates it
in vivo
. These results suggest that continual lymphocyte apoptosis and phagocytosis of apoptotic cells by macrophages have a role in parasite persistence in the host, and that cyclooxygenase inhibitors have potential therapeutic application in the control of parasite replication and spread in Chagas' disease.</description><identifier>ISSN: 0028-0836</identifier><identifier>EISSN: 1476-4687</identifier><identifier>DOI: 10.1038/35003208</identifier><identifier>PMID: 10646605</identifier><identifier>CODEN: NATUAS</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Amino Acid Chloromethyl Ketones - pharmacology ; Animals ; Apoptosis ; Bacteria ; Biosynthesis ; Cells ; Cells, Cultured ; Chagas Disease - immunology ; Chagas Disease - parasitology ; cyclooxygenase inhibitors ; Cysteine Proteinase Inhibitors - pharmacology ; Dinoprostone - biosynthesis ; Dinoprostone - physiology ; Disease ; Humanities and Social Sciences ; letter ; Lymphocytes ; Macrophages - parasitology ; Male ; Mice ; Mice, Inbred BALB C ; multidisciplinary ; Necrosis ; Parasite control ; Phagocytosis - physiology ; Putrescine - biosynthesis ; Putrescine - physiology ; Receptors, Vitronectin - metabolism ; Rodents ; Science ; Science (multidisciplinary) ; T-Lymphocytes - drug effects ; T-Lymphocytes - pathology ; T-Lymphocytes - physiology ; Transforming Growth Factor beta - physiology ; Trypanosoma cruzi ; Trypanosoma cruzi - growth & development ; Vector-borne diseases ; vitronectin receptors</subject><ispartof>Nature (London), 2000-01, Vol.403 (6766), p.199-203</ispartof><rights>Macmillan Magazines Ltd. 2000</rights><rights>COPYRIGHT 2000 Nature Publishing Group</rights><rights>Copyright Macmillan Journals Ltd. Jan 13, 2000</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c675t-f6a3aca75baeff757e1236e70889819b5f0e5422cc658f2701d9f8f07d159c793</citedby><cites>FETCH-LOGICAL-c675t-f6a3aca75baeff757e1236e70889819b5f0e5422cc658f2701d9f8f07d159c793</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/35003208$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/35003208$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10646605$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Freire-de-Lima, Célio G.</creatorcontrib><creatorcontrib>Nascimento, Danielle O.</creatorcontrib><creatorcontrib>Soares, Milena B. P.</creatorcontrib><creatorcontrib>Bozza, Patricia T.</creatorcontrib><creatorcontrib>Castro-Faria-Neto, Hugo C.</creatorcontrib><creatorcontrib>de Mello, Fernando G.</creatorcontrib><creatorcontrib>DosReis, George A.</creatorcontrib><creatorcontrib>Lopes, Marcela F.</creatorcontrib><title>Uptake of apoptotic cells drives the growth of a pathogenic trypanosome in macrophages</title><title>Nature (London)</title><addtitle>Nature</addtitle><addtitle>Nature</addtitle><description>After apoptosis, phagocytes prevent inflammation and tissue damage by the uptake and removal of dead cells
1
. In addition, apoptotic cells evoke an anti-inflammatory response through macrophages
2
,
3
. We have previously shown that there is intense lymphocyte apoptosis in an experimental model of Chagas' disease
4
, a debilitating cardiac illness caused by the protozoan
Trypanosoma cruzi
. Here we show that the interaction of apoptotic, but not necrotic T lymphocytes with macrophages infected with
T. cruzi
fuels parasite growth in a manner dependent on prostaglandins, transforming growth factor-β (TGF-β) and polyamine biosynthesis. We show that the vitronectin receptor is critical, in both apoptotic-cell cytoadherence and the induction of prostaglandin E
2
/TGF-β release and ornithine decarboxylase activity in macrophages. A single injection of apoptotic cells in infected mice increases parasitaemia, whereas treatment with cyclooxygenase inhibitors almost completely ablates it
in vivo
. These results suggest that continual lymphocyte apoptosis and phagocytosis of apoptotic cells by macrophages have a role in parasite persistence in the host, and that cyclooxygenase inhibitors have potential therapeutic application in the control of parasite replication and spread in Chagas' disease.</description><subject>Amino Acid Chloromethyl Ketones - pharmacology</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Bacteria</subject><subject>Biosynthesis</subject><subject>Cells</subject><subject>Cells, Cultured</subject><subject>Chagas Disease - immunology</subject><subject>Chagas Disease - parasitology</subject><subject>cyclooxygenase inhibitors</subject><subject>Cysteine Proteinase Inhibitors - pharmacology</subject><subject>Dinoprostone - biosynthesis</subject><subject>Dinoprostone - physiology</subject><subject>Disease</subject><subject>Humanities and Social Sciences</subject><subject>letter</subject><subject>Lymphocytes</subject><subject>Macrophages - parasitology</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>multidisciplinary</subject><subject>Necrosis</subject><subject>Parasite control</subject><subject>Phagocytosis - physiology</subject><subject>Putrescine - biosynthesis</subject><subject>Putrescine - physiology</subject><subject>Receptors, Vitronectin - metabolism</subject><subject>Rodents</subject><subject>Science</subject><subject>Science (multidisciplinary)</subject><subject>T-Lymphocytes - drug effects</subject><subject>T-Lymphocytes - pathology</subject><subject>T-Lymphocytes - physiology</subject><subject>Transforming Growth Factor beta - physiology</subject><subject>Trypanosoma cruzi</subject><subject>Trypanosoma cruzi - growth & development</subject><subject>Vector-borne diseases</subject><subject>vitronectin receptors</subject><issn>0028-0836</issn><issn>1476-4687</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BEC</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqF0l1v0zAUBuAIgVgZSPwCFHHBh1DGsR1_5LKq-Jg0gQQbXEaue5xmNHFmO8D-PS4t6gpjUy4sJY9fHb05WfaYwBEBpl4zDsAoqDvZhJRSFKVQ8m42AaCqAMXEQfYghHMA4ESW97MDAqIUAvgk-3I2RP0Nc2dzPbghutia3OBqFfKFb79jyOMS88a7H3H5G-WDjkvXYJ9c9JeD7l1wHeZtn3faeDcsdYPhYXbP6lXAR9vzMDt7--Z09r44-fjueDY9KYyQPBZWaKaNlnyu0VrJJRLKBEpQqlKkmnMLyEtKjRFcWSqBLCqrLMgF4ZWRFTvMnm9yB-8uRgyx7tqwHl_36MZQy5KVUBGpknx2swQlBGX0VkgJ41xwuBWmqssKyvWQL26GgijCiZLrzKd_0XM3-j5VWFMoSykpXU9YbFCjV1i3vXXRa5N-CXq9cj3aNr2eEqUI4YyqXeieN0N7UV9FR9eg9Cywa821qS_3LiQT8Wds9BhCffz507599X87Pf06-7Cvt32ldQrBo60H33baX9YE6vW-13_2PdEn277GeYeLK3Cz4LspQ_rUN-h3hf4T9guJYwCf</recordid><startdate>20000113</startdate><enddate>20000113</enddate><creator>Freire-de-Lima, Célio G.</creator><creator>Nascimento, Danielle O.</creator><creator>Soares, Milena B. 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P.</au><au>Bozza, Patricia T.</au><au>Castro-Faria-Neto, Hugo C.</au><au>de Mello, Fernando G.</au><au>DosReis, George A.</au><au>Lopes, Marcela F.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Uptake of apoptotic cells drives the growth of a pathogenic trypanosome in macrophages</atitle><jtitle>Nature (London)</jtitle><stitle>Nature</stitle><addtitle>Nature</addtitle><date>2000-01-13</date><risdate>2000</risdate><volume>403</volume><issue>6766</issue><spage>199</spage><epage>203</epage><pages>199-203</pages><issn>0028-0836</issn><eissn>1476-4687</eissn><coden>NATUAS</coden><abstract>After apoptosis, phagocytes prevent inflammation and tissue damage by the uptake and removal of dead cells
1
. In addition, apoptotic cells evoke an anti-inflammatory response through macrophages
2
,
3
. We have previously shown that there is intense lymphocyte apoptosis in an experimental model of Chagas' disease
4
, a debilitating cardiac illness caused by the protozoan
Trypanosoma cruzi
. Here we show that the interaction of apoptotic, but not necrotic T lymphocytes with macrophages infected with
T. cruzi
fuels parasite growth in a manner dependent on prostaglandins, transforming growth factor-β (TGF-β) and polyamine biosynthesis. We show that the vitronectin receptor is critical, in both apoptotic-cell cytoadherence and the induction of prostaglandin E
2
/TGF-β release and ornithine decarboxylase activity in macrophages. A single injection of apoptotic cells in infected mice increases parasitaemia, whereas treatment with cyclooxygenase inhibitors almost completely ablates it
in vivo
. These results suggest that continual lymphocyte apoptosis and phagocytosis of apoptotic cells by macrophages have a role in parasite persistence in the host, and that cyclooxygenase inhibitors have potential therapeutic application in the control of parasite replication and spread in Chagas' disease.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>10646605</pmid><doi>10.1038/35003208</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0028-0836 |
| ispartof | Nature (London), 2000-01, Vol.403 (6766), p.199-203 |
| issn | 0028-0836 1476-4687 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_743409178 |
| source | MEDLINE; SpringerLink Journals; Nature Journals Online |
| subjects | Amino Acid Chloromethyl Ketones - pharmacology Animals Apoptosis Bacteria Biosynthesis Cells Cells, Cultured Chagas Disease - immunology Chagas Disease - parasitology cyclooxygenase inhibitors Cysteine Proteinase Inhibitors - pharmacology Dinoprostone - biosynthesis Dinoprostone - physiology Disease Humanities and Social Sciences letter Lymphocytes Macrophages - parasitology Male Mice Mice, Inbred BALB C multidisciplinary Necrosis Parasite control Phagocytosis - physiology Putrescine - biosynthesis Putrescine - physiology Receptors, Vitronectin - metabolism Rodents Science Science (multidisciplinary) T-Lymphocytes - drug effects T-Lymphocytes - pathology T-Lymphocytes - physiology Transforming Growth Factor beta - physiology Trypanosoma cruzi Trypanosoma cruzi - growth & development Vector-borne diseases vitronectin receptors |
| title | Uptake of apoptotic cells drives the growth of a pathogenic trypanosome in macrophages |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-09T07%3A19%3A15IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_proqu&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Uptake%20of%20apoptotic%20cells%20drives%20the%20growth%20of%20a%20pathogenic%20trypanosome%20in%20macrophages&rft.jtitle=Nature%20(London)&rft.au=Freire-de-Lima,%20C%C3%A9lio%20G.&rft.date=2000-01-13&rft.volume=403&rft.issue=6766&rft.spage=199&rft.epage=203&rft.pages=199-203&rft.issn=0028-0836&rft.eissn=1476-4687&rft.coden=NATUAS&rft_id=info:doi/10.1038/35003208&rft_dat=%3Cgale_proqu%3EA188115328%3C/gale_proqu%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=204477222&rft_id=info:pmid/10646605&rft_galeid=A188115328&rfr_iscdi=true |