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Salmonella typhimurium Attachment to Human Intestinal Epithelial Monolayers: Transcellular Signalling to Subepithelial Neutrophils
In human intestinal disease induced by Salmonella typhimurium, transepithelial migration of neutrophils (PMN) rapidly follows attachment of the bacteria to the epithelial apical membrane. In this report, we model these interactions in vitro, using polarized monolayers of the human intestinal epithel...
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Published in: | The Journal of cell biology 1993-11, Vol.123 (4), p.895-907 |
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description | In human intestinal disease induced by Salmonella typhimurium, transepithelial migration of neutrophils (PMN) rapidly follows attachment of the bacteria to the epithelial apical membrane. In this report, we model these interactions in vitro, using polarized monolayers of the human intestinal epithelial cell, T84, isolated human PMN, and S. typhimurium. We show that Salmonella attachment to T84 cell apical membranes did not alter monolayer integrity as assessed by transepithelial resistance and measurements of ion transport. However, when human neutrophils were subsequently placed on the basolateral surface of monolayers apically colonized by Salmonella, physiologically directed transepithelial PMN migration ensued. In contrast, attachment of a non-pathogenic Escherichia coli strain to the apical membrane of epithelial cells at comparable densities failed to stimulate a directed PMN transepithelial migration. Use of the n-formyl-peptide receptor antagonist N-t-BOC-1-methionyl-1-leucyl-1-phenylalanine (tBOC-MLP) indicated that the Salmonella-induced PMN transepithelial migration response was not attributable to the classical pathway by which bacteria induce directed migration of PMN. Moreover, the PMN transmigration response required Salmonella adhesion to the epithelial apical membrane and subsequent reciprocal protein synthesis in both bacteria and epithelial cells. Among the events stimulated by this interaction was the epithelial synthesis and polarized release of the potent PMN chemotactic peptide interleukin-8 (IL-8). However, IL-8 neutralization, transfer, and induction experiments indicated that this cytokine was not responsible for the elicited PMN transmigration. These data indicate that a novel transcellular pathway exists in which subepithelial PMN respond to lumenal pathogens across a functionally intact epithelium. Based on the known unique characteristics of the intestinal mucosa, we speculate that IL-8 may act in concert with an as yet unidentified transcellular chemotactic factor(s) (TCF) which directs PMN migration across the intestinal epithelium. |
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In this report, we model these interactions in vitro, using polarized monolayers of the human intestinal epithelial cell, T84, isolated human PMN, and S. typhimurium. We show that Salmonella attachment to T84 cell apical membranes did not alter monolayer integrity as assessed by transepithelial resistance and measurements of ion transport. However, when human neutrophils were subsequently placed on the basolateral surface of monolayers apically colonized by Salmonella, physiologically directed transepithelial PMN migration ensued. In contrast, attachment of a non-pathogenic Escherichia coli strain to the apical membrane of epithelial cells at comparable densities failed to stimulate a directed PMN transepithelial migration. Use of the n-formyl-peptide receptor antagonist N-t-BOC-1-methionyl-1-leucyl-1-phenylalanine (tBOC-MLP) indicated that the Salmonella-induced PMN transepithelial migration response was not attributable to the classical pathway by which bacteria induce directed migration of PMN. Moreover, the PMN transmigration response required Salmonella adhesion to the epithelial apical membrane and subsequent reciprocal protein synthesis in both bacteria and epithelial cells. Among the events stimulated by this interaction was the epithelial synthesis and polarized release of the potent PMN chemotactic peptide interleukin-8 (IL-8). However, IL-8 neutralization, transfer, and induction experiments indicated that this cytokine was not responsible for the elicited PMN transmigration. These data indicate that a novel transcellular pathway exists in which subepithelial PMN respond to lumenal pathogens across a functionally intact epithelium. Based on the known unique characteristics of the intestinal mucosa, we speculate that IL-8 may act in concert with an as yet unidentified transcellular chemotactic factor(s) (TCF) which directs PMN migration across the intestinal epithelium.</description><identifier>ISSN: 0021-9525</identifier><identifier>EISSN: 1540-8140</identifier><identifier>DOI: 10.1083/jcb.123.4.895</identifier><identifier>PMID: 8227148</identifier><identifier>CODEN: JCLBA3</identifier><language>eng</language><publisher>New York, NY: Rockefeller University Press</publisher><subject>Animal migration behavior ; Bacteria ; Bacterial Adhesion - immunology ; Bacterial diseases ; Bacterial Proteins - metabolism ; Biological and medical sciences ; Cell lines ; Cells ; Cells, Cultured ; Cellular biology ; Chemotactic Factors - metabolism ; Chemotaxis, Leukocyte ; Digestive system ; Disease ; Epithelial cells ; Epithelium - metabolism ; Epithelium - microbiology ; Experimental bacterial diseases and models ; Humans ; Infectious diseases ; Interleukin-8 - metabolism ; Intestinal Mucosa - metabolism ; Intestines - cytology ; Intestines - immunology ; Intestines - microbiology ; Medical sciences ; Neutrophils ; Neutrophils - immunology ; Salmonella ; Salmonella typhimurium ; Salmonella typhimurium - immunology ; Secretion ; Signal Transduction ; Transmigration</subject><ispartof>The Journal of cell biology, 1993-11, Vol.123 (4), p.895-907</ispartof><rights>Copyright 1993 The Rockefeller University Press</rights><rights>1994 INIST-CNRS</rights><rights>Copyright Rockefeller University Press Nov 1993</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c459t-714c61880fd07d273127b84b6a14f5d4249f6d5afff226c0a8d83cb5c3c067973</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=3853828$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8227148$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>McCormick, Beth A.</creatorcontrib><creatorcontrib>Colgan, Sean P.</creatorcontrib><creatorcontrib>Delp-Archer, Charlene</creatorcontrib><creatorcontrib>Miller, Samuel I.</creatorcontrib><creatorcontrib>Madara, James L.</creatorcontrib><title>Salmonella typhimurium Attachment to Human Intestinal Epithelial Monolayers: Transcellular Signalling to Subepithelial Neutrophils</title><title>The Journal of cell biology</title><addtitle>J Cell Biol</addtitle><description>In human intestinal disease induced by Salmonella typhimurium, transepithelial migration of neutrophils (PMN) rapidly follows attachment of the bacteria to the epithelial apical membrane. In this report, we model these interactions in vitro, using polarized monolayers of the human intestinal epithelial cell, T84, isolated human PMN, and S. typhimurium. We show that Salmonella attachment to T84 cell apical membranes did not alter monolayer integrity as assessed by transepithelial resistance and measurements of ion transport. However, when human neutrophils were subsequently placed on the basolateral surface of monolayers apically colonized by Salmonella, physiologically directed transepithelial PMN migration ensued. In contrast, attachment of a non-pathogenic Escherichia coli strain to the apical membrane of epithelial cells at comparable densities failed to stimulate a directed PMN transepithelial migration. Use of the n-formyl-peptide receptor antagonist N-t-BOC-1-methionyl-1-leucyl-1-phenylalanine (tBOC-MLP) indicated that the Salmonella-induced PMN transepithelial migration response was not attributable to the classical pathway by which bacteria induce directed migration of PMN. Moreover, the PMN transmigration response required Salmonella adhesion to the epithelial apical membrane and subsequent reciprocal protein synthesis in both bacteria and epithelial cells. Among the events stimulated by this interaction was the epithelial synthesis and polarized release of the potent PMN chemotactic peptide interleukin-8 (IL-8). However, IL-8 neutralization, transfer, and induction experiments indicated that this cytokine was not responsible for the elicited PMN transmigration. These data indicate that a novel transcellular pathway exists in which subepithelial PMN respond to lumenal pathogens across a functionally intact epithelium. Based on the known unique characteristics of the intestinal mucosa, we speculate that IL-8 may act in concert with an as yet unidentified transcellular chemotactic factor(s) (TCF) which directs PMN migration across the intestinal epithelium.</description><subject>Animal migration behavior</subject><subject>Bacteria</subject><subject>Bacterial Adhesion - immunology</subject><subject>Bacterial diseases</subject><subject>Bacterial Proteins - metabolism</subject><subject>Biological and medical sciences</subject><subject>Cell lines</subject><subject>Cells</subject><subject>Cells, Cultured</subject><subject>Cellular biology</subject><subject>Chemotactic Factors - metabolism</subject><subject>Chemotaxis, Leukocyte</subject><subject>Digestive system</subject><subject>Disease</subject><subject>Epithelial cells</subject><subject>Epithelium - metabolism</subject><subject>Epithelium - microbiology</subject><subject>Experimental bacterial diseases and models</subject><subject>Humans</subject><subject>Infectious diseases</subject><subject>Interleukin-8 - metabolism</subject><subject>Intestinal Mucosa - metabolism</subject><subject>Intestines - cytology</subject><subject>Intestines - immunology</subject><subject>Intestines - microbiology</subject><subject>Medical sciences</subject><subject>Neutrophils</subject><subject>Neutrophils - immunology</subject><subject>Salmonella</subject><subject>Salmonella typhimurium</subject><subject>Salmonella typhimurium - immunology</subject><subject>Secretion</subject><subject>Signal Transduction</subject><subject>Transmigration</subject><issn>0021-9525</issn><issn>1540-8140</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1993</creationdate><recordtype>article</recordtype><recordid>eNpdkUtvEzEURi0EKiFlyQ6kUYXYTern2MOiUlUVWqnAImVteTyexJFnHPxAypZfjkOiFFjZ0j3-fO89ALxBcIGgIJcb3S0QJgu6EC17BmaIUVgLROFzMIMQo7plmL0Er2LcQAgpp-QMnAmMOaJiBn4tlRv9ZJxTVdpt13bMweaxuk5J6fVoplQlX93lUU3V_ZRMTHZSrrrd2rQ2zpbrFz95p3YmxI_VY1BT1CUsOxWqpV0V1tlptc9Y5s48vfpqcgq-_OfiOXgxKBfN6-M5B98_3T7e3NUP3z7f31w_1JqyNtWlX90gIeDQQ95jThDmnaBdoxAdWE8xbYemZ2oYBowbDZXoBdEd00TDhreczMHVIXebu9H0uswWlJPbYEcVdtIrK_-tTHYtV_6nxBhCxPYBH44Bwf_IZRVytH-mVZPxOUreQIZ52xTw4j9w43Mou4gSIw5byIu4OagPkA4-xmCGUycIyr1ZWczKYlZSWcwW_t3f7Z_oo8pSf3-sq6iVG4oKbeMJI4IRgffY2wO2icmHpz8bxFoGyW_ZILjd</recordid><startdate>19931101</startdate><enddate>19931101</enddate><creator>McCormick, Beth A.</creator><creator>Colgan, Sean P.</creator><creator>Delp-Archer, Charlene</creator><creator>Miller, Samuel I.</creator><creator>Madara, James L.</creator><general>Rockefeller University Press</general><general>The Rockefeller University Press</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>7QL</scope><scope>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>M7N</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>19931101</creationdate><title>Salmonella typhimurium Attachment to Human Intestinal Epithelial Monolayers: Transcellular Signalling to Subepithelial Neutrophils</title><author>McCormick, Beth A. ; Colgan, Sean P. ; Delp-Archer, Charlene ; Miller, Samuel I. ; Madara, James L.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c459t-714c61880fd07d273127b84b6a14f5d4249f6d5afff226c0a8d83cb5c3c067973</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1993</creationdate><topic>Animal migration behavior</topic><topic>Bacteria</topic><topic>Bacterial Adhesion - immunology</topic><topic>Bacterial diseases</topic><topic>Bacterial Proteins - metabolism</topic><topic>Biological and medical sciences</topic><topic>Cell lines</topic><topic>Cells</topic><topic>Cells, Cultured</topic><topic>Cellular biology</topic><topic>Chemotactic Factors - metabolism</topic><topic>Chemotaxis, Leukocyte</topic><topic>Digestive system</topic><topic>Disease</topic><topic>Epithelial cells</topic><topic>Epithelium - metabolism</topic><topic>Epithelium - microbiology</topic><topic>Experimental bacterial diseases and models</topic><topic>Humans</topic><topic>Infectious diseases</topic><topic>Interleukin-8 - metabolism</topic><topic>Intestinal Mucosa - metabolism</topic><topic>Intestines - cytology</topic><topic>Intestines - immunology</topic><topic>Intestines - microbiology</topic><topic>Medical sciences</topic><topic>Neutrophils</topic><topic>Neutrophils - immunology</topic><topic>Salmonella</topic><topic>Salmonella typhimurium</topic><topic>Salmonella typhimurium - immunology</topic><topic>Secretion</topic><topic>Signal Transduction</topic><topic>Transmigration</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>McCormick, Beth A.</creatorcontrib><creatorcontrib>Colgan, Sean P.</creatorcontrib><creatorcontrib>Delp-Archer, Charlene</creatorcontrib><creatorcontrib>Miller, Samuel I.</creatorcontrib><creatorcontrib>Madara, James L.</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>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of cell biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>McCormick, Beth A.</au><au>Colgan, Sean P.</au><au>Delp-Archer, Charlene</au><au>Miller, Samuel I.</au><au>Madara, James L.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Salmonella typhimurium Attachment to Human Intestinal Epithelial Monolayers: Transcellular Signalling to Subepithelial Neutrophils</atitle><jtitle>The Journal of cell biology</jtitle><addtitle>J Cell Biol</addtitle><date>1993-11-01</date><risdate>1993</risdate><volume>123</volume><issue>4</issue><spage>895</spage><epage>907</epage><pages>895-907</pages><issn>0021-9525</issn><eissn>1540-8140</eissn><coden>JCLBA3</coden><abstract>In human intestinal disease induced by Salmonella typhimurium, transepithelial migration of neutrophils (PMN) rapidly follows attachment of the bacteria to the epithelial apical membrane. In this report, we model these interactions in vitro, using polarized monolayers of the human intestinal epithelial cell, T84, isolated human PMN, and S. typhimurium. We show that Salmonella attachment to T84 cell apical membranes did not alter monolayer integrity as assessed by transepithelial resistance and measurements of ion transport. However, when human neutrophils were subsequently placed on the basolateral surface of monolayers apically colonized by Salmonella, physiologically directed transepithelial PMN migration ensued. In contrast, attachment of a non-pathogenic Escherichia coli strain to the apical membrane of epithelial cells at comparable densities failed to stimulate a directed PMN transepithelial migration. Use of the n-formyl-peptide receptor antagonist N-t-BOC-1-methionyl-1-leucyl-1-phenylalanine (tBOC-MLP) indicated that the Salmonella-induced PMN transepithelial migration response was not attributable to the classical pathway by which bacteria induce directed migration of PMN. Moreover, the PMN transmigration response required Salmonella adhesion to the epithelial apical membrane and subsequent reciprocal protein synthesis in both bacteria and epithelial cells. Among the events stimulated by this interaction was the epithelial synthesis and polarized release of the potent PMN chemotactic peptide interleukin-8 (IL-8). However, IL-8 neutralization, transfer, and induction experiments indicated that this cytokine was not responsible for the elicited PMN transmigration. These data indicate that a novel transcellular pathway exists in which subepithelial PMN respond to lumenal pathogens across a functionally intact epithelium. Based on the known unique characteristics of the intestinal mucosa, we speculate that IL-8 may act in concert with an as yet unidentified transcellular chemotactic factor(s) (TCF) which directs PMN migration across the intestinal epithelium.</abstract><cop>New York, NY</cop><pub>Rockefeller University Press</pub><pmid>8227148</pmid><doi>10.1083/jcb.123.4.895</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animal migration behavior Bacteria Bacterial Adhesion - immunology Bacterial diseases Bacterial Proteins - metabolism Biological and medical sciences Cell lines Cells Cells, Cultured Cellular biology Chemotactic Factors - metabolism Chemotaxis, Leukocyte Digestive system Disease Epithelial cells Epithelium - metabolism Epithelium - microbiology Experimental bacterial diseases and models Humans Infectious diseases Interleukin-8 - metabolism Intestinal Mucosa - metabolism Intestines - cytology Intestines - immunology Intestines - microbiology Medical sciences Neutrophils Neutrophils - immunology Salmonella Salmonella typhimurium Salmonella typhimurium - immunology Secretion Signal Transduction Transmigration |
title | Salmonella typhimurium Attachment to Human Intestinal Epithelial Monolayers: Transcellular Signalling to Subepithelial Neutrophils |
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