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This lEV release was inhibited when IP\n                    <jats:sub>3<\/jats:sub>\n                    \u2010mediated Ca\n                    <jats:sup>2+<\/jats:sup>\n                    exit from the ER and further Ca\n                    <jats:sup>2+<\/jats:sup>\n                    entry from plasma membrane channels was blocked, but whilst any store\u2010independent Ca\n                    <jats:sup>2+<\/jats:sup>\n                    entry (SICE) could continue unabated. That lEV release was equally inhibited if all entry from external sources was blocked by chelation of external Ca\n                    <jats:sup>2+<\/jats:sup>\n                    points to the major contributor to Mtr\u2010triggered host cell lEV release being IP\n                    <jats:sub>3<\/jats:sub>\n                    \/store\u2010mediated Ca\n                    <jats:sup>2+<\/jats:sup>\n                    release, SICE playing a minor role. Host cell lEVs were released through Mtr interaction with host cell lipid raft domains, integrins, and mechanosensitive ion channels, whereupon [Ca\n                    <jats:sup>2+<\/jats:sup>\n                    ]\n                    <jats:sub>cyt<\/jats:sub>\n                    increased (50 to 750\u00a0nM) within 15 s. lEV release and cell entry of\n                    <jats:italic>T. cruzi<\/jats:italic>\n                    , which increased up to 30 and 60 mpi, respectively, as well as raised actin depolymerization at 60 mpi, were all reduced by TRPC inhibitor, GsMTx\u20104. Vesicle release and infection was also reduced with RGD peptide, methyl\u2010\u03b2\u2010cyclodextrin, knockdown of calpain and with the calpain inhibitor, calpeptin. Restoration of lEV levels, whether with lEVs from infected or uninfected epithelial cells, did not restore invasion, but supplementation with lEVs from infected monocytes, did. We provide evidence of THP\u20101 monocyte\u2010derived lEV interaction with Mtr (lipid mixing by R18\u2010dequenching; flow cytometry showing transfer to Mtr of R18 from R18\u2010lEVs and of LAP(TGF\u2010\u03b21). Active, mature TGF\u2010\u03b21 (at 175 pg\/\u00d710\n                    <jats:sup>5<\/jats:sup>\n                    in THP\u20101 lEVs) was detected in concentrated lEV\u2010\/cell\u2010free supernatant by western blotting, only after THP\u20101 lEVs had interacted with Mtr. The TGF\u2010\u03b21 receptor (T\u03b2RI) inhibitor, SB\u2010431542, reduced the enhanced cellular invasion due to monocyte\u2010lEVs.\n                  <\/jats:p>","DOI":"10.1002\/jev2.70014","type":"journal-article","created":{"date-parts":[[2024,11,29]],"date-time":"2024-11-29T06:30:28Z","timestamp":1732861828000},"source":"Crossref","is-referenced-by-count":7,"title":["Monocyte\u2010derived extracellular vesicles, stimulated by\n                    <i>Trypanosoma cruzi<\/i>\n                    , enhance cellular invasion\n                    <i>in\u00a0vitro<\/i>\n                    via activated TGF\u2010\u03b21"],"prefix":"10.1002","volume":"13","author":[{"given":"Ephraim A.","family":"Ansa\u2010Addo","sequence":"first","affiliation":[{"name":"School of Human Sciences, Cell Communication in Disease Pathology London Metropolitan University London UK"},{"name":"Pelotonia Institute for Immuno\u2010Oncology, Department of Internal Medicine The Ohio State University Comprehensive Cancer Center Columbus Ohio USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paras","family":"Pathak","sequence":"additional","affiliation":[{"name":"School of Human Sciences, Cell Communication in Disease Pathology London Metropolitan University London UK"},{"name":"Medical Research Council Harwell Harwell Science and Innovation Campus, Genotyping Core Oxfordshire UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maria V.","family":"McCrossan","sequence":"additional","affiliation":[{"name":"Immunology Unit London School of Hygiene and Tropical Medicine London UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Izadora","family":"Volpato Rossi","sequence":"additional","affiliation":[{"name":"School of Human Sciences, Cell Communication in Disease Pathology London Metropolitan University London UK"},{"name":"School of Life and Medical Sciences, Biosciences Research Group University of Hertfordshire Hatfield UK"},{"name":"Carlos Chagas Institute Fundacao Oswaldo Cruz, (FIOCRUZ\u2010PR) Curitiba Brazil"},{"name":"Postgraduate Program in Cellular and Molecular Biology Federal University of Paran\u00e1 Curitiba Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mahamed","family":"Abdullahi","sequence":"additional","affiliation":[{"name":"School of Human Sciences, Cell Communication in Disease Pathology London Metropolitan University London UK"},{"name":"National Mycobacterium Reference Service\u2010South (NMRS\u2010South) Colindale London UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dan","family":"Stratton","sequence":"additional","affiliation":[{"name":"School of Life, Health &amp; Chemical Sciences The Open University Milton Keynes UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sigrun","family":"Lange","sequence":"additional","affiliation":[{"name":"Tissue Architecture and Regeneration Research Group, School of Life Sciences University of Westminster London UK"},{"name":"University College London, Institute of Women's Health London UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marcel I.","family":"Ramirez","sequence":"additional","affiliation":[{"name":"Carlos Chagas Institute Fundacao Oswaldo Cruz, (FIOCRUZ\u2010PR) Curitiba Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7200-0363","authenticated-orcid":false,"given":"Jameel M.","family":"Inal","sequence":"additional","affiliation":[{"name":"School of Human Sciences, Cell Communication in Disease Pathology London Metropolitan University London UK"},{"name":"School of Life and Medical Sciences, Biosciences Research Group University of Hertfordshire Hatfield UK"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2024,11,29]]},"reference":[{"key":"e_1_2_9_2_1","doi-asserted-by":"publisher","DOI":"10.1177\/002215540205001010"},{"key":"e_1_2_9_3_1","doi-asserted-by":"publisher","DOI":"10.1038\/ncb1725"},{"key":"e_1_2_9_4_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.ceca.2016.12.009"},{"key":"e_1_2_9_5_1","doi-asserted-by":"publisher","DOI":"10.4049\/jimmunol.1001656"},{"key":"e_1_2_9_6_1","doi-asserted-by":"publisher","DOI":"10.1080\/20013078.2019.1697124"},{"key":"e_1_2_9_7_1","first-page":"77","article-title":"Calcium signaling through phospholipase C activates dendritic cells to mature and is necessary for the activation and maturation of dendritic cells induced by diverse agonists","volume":"11","author":"Bagley K. 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