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The infection process of Piscirickettsia salmonis in fish macrophages is dependent upon interaction with host-cell clathrin and actin
Piscirickettsia salmonis is an aggressive fish pathogen that causes Piscirickettsiosis, a systemic disease that threatens the sustainability of salmon production in Chile. To date, the infection strategies of this bacterium are poorly characterized, a Dot/Icm Type IV Secretion System homolog for int...
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Published in: | FEMS microbiology letters 2015-01, Vol.362 (1), p.1-8 |
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description | Piscirickettsia salmonis is an aggressive fish pathogen that causes Piscirickettsiosis, a systemic disease that threatens the sustainability of salmon production in Chile. To date, the infection strategies of this bacterium are poorly characterized, a Dot/Icm Type IV Secretion System homolog for intracellular multiplication and survival in macrophages is suggested. Since an invading pathogen and its host develop a complex interaction in which the pathogen strives to survive and replicate, while the host tries to eliminate infected cells and the invading pathogen, we decided to evaluate how the bacterium enters macrophages, its preferred target in vivo, and to follow its fate while struggling with its host using actin cytoskeleton as a molecular marker. We were able to demonstrate that clathrin is required for internalization and that actin cytoskeleton plays a demonstrative role throughout the infective process. Indeed, unlike other fish pathogens, P. salmonis fully exploits the actin monomers both from the disorganized cytoskeleton and an apparently pathogen-induced de novo synthesis of actin, generating tridimensional vacuoles that are increasingly detected at later stages of infection. We expect our results to contribute to a better understanding of the pathogenesis of this important fish pathogen.
In this work was able to confirm that P. salmonis, an important fish pathogen of salmon industry, require host-cell actin and clathrin to infect macrophages. Clathrin is required for inicial internalization and the actin participes in the formation of a replicative vacuole. |
doi_str_mv | 10.1093/femsle/fnu012 |
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In this work was able to confirm that P. salmonis, an important fish pathogen of salmon industry, require host-cell actin and clathrin to infect macrophages. Clathrin is required for inicial internalization and the actin participes in the formation of a replicative vacuole.</description><identifier>ISSN: 1574-6968</identifier><identifier>ISSN: 0378-1097</identifier><identifier>EISSN: 1574-6968</identifier><identifier>DOI: 10.1093/femsle/fnu012</identifier><identifier>PMID: 25790493</identifier><language>eng</language><publisher>England: Oxford University Press</publisher><subject>Actin ; Actins - metabolism ; Animals ; Bacteria ; Cell Line ; Chile ; Clathrin ; Clathrin - metabolism ; Cytoskeleton ; Endocytosis ; Fish ; Homology ; Host-Pathogen Interactions ; Infections ; Internalization ; Macrophages ; Macrophages - microbiology ; Microbiology ; Monomers ; Multiplication ; Pathogenesis ; Pathogens ; Piscirickettsia - physiology ; Piscirickettsia salmonis ; Salmon ; Secretion ; Vacuoles</subject><ispartof>FEMS microbiology letters, 2015-01, Vol.362 (1), p.1-8</ispartof><rights>FEMS 2014. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com 2014</rights><rights>FEMS 2014. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.</rights><rights>FEMS 2014. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c354t-3ea07d1fbcde255dab77a632a4842f8513791fa63c3b59926e3b51f26a8e8d473</citedby><cites>FETCH-LOGICAL-c354t-3ea07d1fbcde255dab77a632a4842f8513791fa63c3b59926e3b51f26a8e8d473</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25790493$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ramírez, Ramón</creatorcontrib><creatorcontrib>Gómez, Fernando A.</creatorcontrib><creatorcontrib>Marshall, Sergio H.</creatorcontrib><title>The infection process of Piscirickettsia salmonis in fish macrophages is dependent upon interaction with host-cell clathrin and actin</title><title>FEMS microbiology letters</title><addtitle>FEMS Microbiol Lett</addtitle><description>Piscirickettsia salmonis is an aggressive fish pathogen that causes Piscirickettsiosis, a systemic disease that threatens the sustainability of salmon production in Chile. To date, the infection strategies of this bacterium are poorly characterized, a Dot/Icm Type IV Secretion System homolog for intracellular multiplication and survival in macrophages is suggested. Since an invading pathogen and its host develop a complex interaction in which the pathogen strives to survive and replicate, while the host tries to eliminate infected cells and the invading pathogen, we decided to evaluate how the bacterium enters macrophages, its preferred target in vivo, and to follow its fate while struggling with its host using actin cytoskeleton as a molecular marker. We were able to demonstrate that clathrin is required for internalization and that actin cytoskeleton plays a demonstrative role throughout the infective process. Indeed, unlike other fish pathogens, P. salmonis fully exploits the actin monomers both from the disorganized cytoskeleton and an apparently pathogen-induced de novo synthesis of actin, generating tridimensional vacuoles that are increasingly detected at later stages of infection. We expect our results to contribute to a better understanding of the pathogenesis of this important fish pathogen.
In this work was able to confirm that P. salmonis, an important fish pathogen of salmon industry, require host-cell actin and clathrin to infect macrophages. Clathrin is required for inicial internalization and the actin participes in the formation of a replicative vacuole.</description><subject>Actin</subject><subject>Actins - metabolism</subject><subject>Animals</subject><subject>Bacteria</subject><subject>Cell Line</subject><subject>Chile</subject><subject>Clathrin</subject><subject>Clathrin - metabolism</subject><subject>Cytoskeleton</subject><subject>Endocytosis</subject><subject>Fish</subject><subject>Homology</subject><subject>Host-Pathogen Interactions</subject><subject>Infections</subject><subject>Internalization</subject><subject>Macrophages</subject><subject>Macrophages - microbiology</subject><subject>Microbiology</subject><subject>Monomers</subject><subject>Multiplication</subject><subject>Pathogenesis</subject><subject>Pathogens</subject><subject>Piscirickettsia - physiology</subject><subject>Piscirickettsia salmonis</subject><subject>Salmon</subject><subject>Secretion</subject><subject>Vacuoles</subject><issn>1574-6968</issn><issn>0378-1097</issn><issn>1574-6968</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><recordid>eNqFkctO3jAQRq2qqFDaZbfIUjfdBHyJk3hZod4kJFjAOvLvjIlpYgePo4oH4L3rX4EWddPVWKOjo2_8EfKBs1POtDxzMOMEZy6sjItX5Iirtq4a3XSvX7wPyVvEO8ZYLVjzhhwK1WpWa3lEHq9HoD44sNnHQJcULSDS6OiVR-uTtz8hZ_SGopnmGDwWmjqPI52NTXEZzS2UHdIBFggDhEzXpZh8yJDMZv3l80jHiLmyME3UTiaPqWhMGOgeCe_IgTMTwvuneUxuvn65Pv9eXVx--3H--aKyUtW5kmBYO3C3swMIpQaza1vTSGHqrhauU1y2mruysXKntBYNlMmdaEwH3VC38ph82rzlzvsVMPdzubJkMgHiij1vGsWFkHqPfvwHvYtrCiVdLyRTStVc6EJVG1W-AjGB65fkZ5Mees76fT_91k-_9VP4kyfrupth-EM_F_I3YVyX_7h-A-Q-nbU</recordid><startdate>20150101</startdate><enddate>20150101</enddate><creator>Ramírez, Ramón</creator><creator>Gómez, Fernando A.</creator><creator>Marshall, Sergio H.</creator><general>Oxford University Press</general><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>7QL</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</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>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>H94</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>RC3</scope><scope>7X8</scope></search><sort><creationdate>20150101</creationdate><title>The infection process of Piscirickettsia salmonis in fish macrophages is dependent upon interaction with host-cell clathrin and actin</title><author>Ramírez, Ramón ; Gómez, Fernando A. ; Marshall, Sergio H.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c354t-3ea07d1fbcde255dab77a632a4842f8513791fa63c3b59926e3b51f26a8e8d473</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Actin</topic><topic>Actins - metabolism</topic><topic>Animals</topic><topic>Bacteria</topic><topic>Cell Line</topic><topic>Chile</topic><topic>Clathrin</topic><topic>Clathrin - metabolism</topic><topic>Cytoskeleton</topic><topic>Endocytosis</topic><topic>Fish</topic><topic>Homology</topic><topic>Host-Pathogen Interactions</topic><topic>Infections</topic><topic>Internalization</topic><topic>Macrophages</topic><topic>Macrophages - microbiology</topic><topic>Microbiology</topic><topic>Monomers</topic><topic>Multiplication</topic><topic>Pathogenesis</topic><topic>Pathogens</topic><topic>Piscirickettsia - physiology</topic><topic>Piscirickettsia salmonis</topic><topic>Salmon</topic><topic>Secretion</topic><topic>Vacuoles</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ramírez, Ramón</creatorcontrib><creatorcontrib>Gómez, Fernando A.</creatorcontrib><creatorcontrib>Marshall, Sergio H.</creatorcontrib><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>Bacteriology Abstracts (Microbiology B)</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>ProQuest Health and Medical</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>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 Central UK/Ireland</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>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biological Sciences</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</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>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>FEMS microbiology letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ramírez, Ramón</au><au>Gómez, Fernando A.</au><au>Marshall, Sergio H.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The infection process of Piscirickettsia salmonis in fish macrophages is dependent upon interaction with host-cell clathrin and actin</atitle><jtitle>FEMS microbiology letters</jtitle><addtitle>FEMS Microbiol Lett</addtitle><date>2015-01-01</date><risdate>2015</risdate><volume>362</volume><issue>1</issue><spage>1</spage><epage>8</epage><pages>1-8</pages><issn>1574-6968</issn><issn>0378-1097</issn><eissn>1574-6968</eissn><abstract>Piscirickettsia salmonis is an aggressive fish pathogen that causes Piscirickettsiosis, a systemic disease that threatens the sustainability of salmon production in Chile. To date, the infection strategies of this bacterium are poorly characterized, a Dot/Icm Type IV Secretion System homolog for intracellular multiplication and survival in macrophages is suggested. Since an invading pathogen and its host develop a complex interaction in which the pathogen strives to survive and replicate, while the host tries to eliminate infected cells and the invading pathogen, we decided to evaluate how the bacterium enters macrophages, its preferred target in vivo, and to follow its fate while struggling with its host using actin cytoskeleton as a molecular marker. We were able to demonstrate that clathrin is required for internalization and that actin cytoskeleton plays a demonstrative role throughout the infective process. Indeed, unlike other fish pathogens, P. salmonis fully exploits the actin monomers both from the disorganized cytoskeleton and an apparently pathogen-induced de novo synthesis of actin, generating tridimensional vacuoles that are increasingly detected at later stages of infection. We expect our results to contribute to a better understanding of the pathogenesis of this important fish pathogen.
In this work was able to confirm that P. salmonis, an important fish pathogen of salmon industry, require host-cell actin and clathrin to infect macrophages. Clathrin is required for inicial internalization and the actin participes in the formation of a replicative vacuole.</abstract><cop>England</cop><pub>Oxford University Press</pub><pmid>25790493</pmid><doi>10.1093/femsle/fnu012</doi><tpages>8</tpages></addata></record> |
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subjects | Actin Actins - metabolism Animals Bacteria Cell Line Chile Clathrin Clathrin - metabolism Cytoskeleton Endocytosis Fish Homology Host-Pathogen Interactions Infections Internalization Macrophages Macrophages - microbiology Microbiology Monomers Multiplication Pathogenesis Pathogens Piscirickettsia - physiology Piscirickettsia salmonis Salmon Secretion Vacuoles |
title | The infection process of Piscirickettsia salmonis in fish macrophages is dependent upon interaction with host-cell clathrin and actin |
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