{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,5]],"date-time":"2025-10-05T16:53:08Z","timestamp":1759683188297},"reference-count":41,"publisher":"American Society for Microbiology","issue":"12","license":[{"start":{"date-parts":[[2010,12,1]],"date-time":"2010-12-01T00:00:00Z","timestamp":1291161600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2010,12]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            The enteric protozoan parasite\n            <jats:italic>Entamoeba histolytica<\/jats:italic>\n            causes amebic colitis through disruption of the mucus layer, followed by binding to and destruction of epithelial cells. However, it is not known whether ameba infections or ameba components can directly affect the enteric nervous system. Analysis of mucosal innervations in the mouse model of cecal amebiasis showed that axon density was diminished to less than 25% of control. To determine whether amebas directly contributed to axon loss, we tested the effect of either\n            <jats:italic>E. histolytica<\/jats:italic>\n            secreted products (Eh-SEC) or soluble components (Eh-SOL) to an established coculture model of myenteric neurons, glia, and smooth muscle cells. Neuronal survival and axonal degeneration were measured after 48 h of exposure to graded doses of Eh-SEC or Eh-SOL (10 to 80 \u03bcg\/ml). The addition of 80 \u03bcg of either component\/ml decreased the neuron number by 30%, whereas the axon number was decreased by 50%. Cytotoxicity was specific to the neuronal population, since the glial and smooth muscle cell number remained similar to that of the control, and was completely abrogated by prior heat denaturation. Neuronal damage was partially prevented by the cysteine protease inhibitor E-64, showing that a heat-labile protease was involved.\n            <jats:italic>E. histolytica<\/jats:italic>\n            lysates derived from amebas deficient in the major secreted protease\n            <jats:italic>EhCP5<\/jats:italic>\n            caused a neurotoxicity similar to that of wild-type amebas. We conclude that\n            <jats:italic>E. histolytica<\/jats:italic>\n            infection and ameba protease activity can cause selective damage to enteric neurons.\n          <\/jats:p>","DOI":"10.1128\/iai.00699-10","type":"journal-article","created":{"date-parts":[[2010,9,21]],"date-time":"2010-09-21T04:10:41Z","timestamp":1285042241000},"page":"5332-5340","update-policy":"http:\/\/dx.doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":25,"title":["<i>Entamoeba histolytica<\/i>\n            Infection and Secreted Proteins Proteolytically Damage Enteric Neurons"],"prefix":"10.1128","volume":"78","author":[{"given":"Sandra","family":"Lourenssen","sequence":"first","affiliation":[{"name":"Gastrointestinal Diseases Research Unit, Queen's University, Kingston, Ontario, Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Eric R.","family":"Houpt","sequence":"additional","affiliation":[{"name":"Division of Infectious Diseases, University of Virginia, Charlottesville, Virginia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kris","family":"Chadee","sequence":"additional","affiliation":[{"name":"Gastrointestinal Research Group, University of Calgary, Calgary, Alberta, Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Michael G.","family":"Blennerhassett","sequence":"additional","affiliation":[{"name":"Gastrointestinal Diseases Research Unit, Queen's University, Kingston, Ontario, Canada"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1002\/jnr.21903"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1128\/iai.65.9.3615-3621.1997"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpgi.2000.279.3.G511"},{"key":"e_1_3_2_5_2","first-page":"G1041","volume":"262","year":"1992","unstructured":"Blennerhassett, M. 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