Bacteria–autophagy interplay: a battle for survival
Key Points Autophagy is used by the cell to degrade various substrates; this is achieved either through the canonical, non-selective autophagy pathway or through selective autophagy. Both pathways proceed via distinct key steps and use specific molecular mechanisms. The canonical autophagy pathway h...
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Veröffentlicht in: | Nature reviews. Microbiology 2014-02, Vol.12 (2), p.101-114 |
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description | Key Points
Autophagy is used by the cell to degrade various substrates; this is achieved either through the canonical, non-selective autophagy pathway or through selective autophagy. Both pathways proceed via distinct key steps and use specific molecular mechanisms.
The canonical autophagy pathway has been studied in detail in mammalian cells and in model organisms, such as yeast. The molecular mechanisms underlying non-canonical autophagy, in addition to alternative pathways that are independent of some of the key autophagy machinery, are beginning to become clear.
Besides degradation of cellular proteins, autophagy proteins are also involved in many other functions, some of which are important during bacterial infections.
Autophagy functions as an antibacterial mechanism. The induction and recognition mechanisms for several bacterial species have been elucidated.
Bacteria can escape killing by autophagy and some can even use autophagy to promote infection of host cells, through the interaction between bacterial effector proteins and autophagy components.
The knowledge about bacteria–autophagy interactions will inform the design of new drugs and treatments against bacterial infections.
Autophagy not only degrades components of host cells but can also target intracellular bacteria and thus contribute to host defences. Here, Huang and Brumell discuss the canonical and selective pathways of antibacterial autophagy, as well as the ways in which bacteria can escape from them and sometimes even use them to promote infection.
Autophagy is a cellular process that targets proteins, lipids and organelles to lysosomes for degradation, but it has also been shown to combat infection with various pathogenic bacteria. In turn, bacteria have developed diverse strategies to avoid autophagy by interfering with autophagy signalling or the autophagy machinery and, in some cases, they even exploit autophagy for their growth. In this Review, we discuss canonical and non-canonical autophagy pathways and our current knowledge of antibacterial autophagy, with a focus on the interplay between bacterial factors and autophagy components. |
doi_str_mv | 10.1038/nrmicro3160 |
format | Article |
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Autophagy is used by the cell to degrade various substrates; this is achieved either through the canonical, non-selective autophagy pathway or through selective autophagy. Both pathways proceed via distinct key steps and use specific molecular mechanisms.
The canonical autophagy pathway has been studied in detail in mammalian cells and in model organisms, such as yeast. The molecular mechanisms underlying non-canonical autophagy, in addition to alternative pathways that are independent of some of the key autophagy machinery, are beginning to become clear.
Besides degradation of cellular proteins, autophagy proteins are also involved in many other functions, some of which are important during bacterial infections.
Autophagy functions as an antibacterial mechanism. The induction and recognition mechanisms for several bacterial species have been elucidated.
Bacteria can escape killing by autophagy and some can even use autophagy to promote infection of host cells, through the interaction between bacterial effector proteins and autophagy components.
The knowledge about bacteria–autophagy interactions will inform the design of new drugs and treatments against bacterial infections.
Autophagy not only degrades components of host cells but can also target intracellular bacteria and thus contribute to host defences. Here, Huang and Brumell discuss the canonical and selective pathways of antibacterial autophagy, as well as the ways in which bacteria can escape from them and sometimes even use them to promote infection.
Autophagy is a cellular process that targets proteins, lipids and organelles to lysosomes for degradation, but it has also been shown to combat infection with various pathogenic bacteria. In turn, bacteria have developed diverse strategies to avoid autophagy by interfering with autophagy signalling or the autophagy machinery and, in some cases, they even exploit autophagy for their growth. In this Review, we discuss canonical and non-canonical autophagy pathways and our current knowledge of antibacterial autophagy, with a focus on the interplay between bacterial factors and autophagy components.</description><identifier>ISSN: 1740-1526</identifier><identifier>EISSN: 1740-1534</identifier><identifier>DOI: 10.1038/nrmicro3160</identifier><identifier>PMID: 24384599</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>631/326/41/2531 ; 631/326/41/2533 ; 631/326/41/2534 ; 631/80/39 ; Antigen presentation ; Antiinfectives and antibacterials ; Apoptosis ; Autophagy ; Autophagy (Cytology) ; Autophagy - physiology ; Bacteria ; Bacteria - pathogenicity ; Bacterial diseases ; Bacterial infections ; Biodegradation ; Cell cycle ; Cell research ; Cell survival ; Cellular control mechanisms ; Cytokines ; Drug development ; Drug interaction ; Effector cells ; Host-Pathogen Interactions ; Infectious Diseases ; Kinases ; Life Sciences ; Lipids ; Lysosomes - metabolism ; Lysosomes - microbiology ; Mammalian cells ; Medical Microbiology ; Microbiology ; Molecular modelling ; Parasitology ; Phagocytosis ; Phagosomes - metabolism ; Phagosomes - microbiology ; Physiological aspects ; Proteins ; Protozoa ; review-article ; Virology ; Yeasts</subject><ispartof>Nature reviews. Microbiology, 2014-02, Vol.12 (2), p.101-114</ispartof><rights>Springer Nature Limited 2014</rights><rights>COPYRIGHT 2014 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Feb 2014</rights><rights>Nature Publishing Group, a division of Macmillan Publishers Limited. All Rights Reserved. 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c640t-e86c2b30e770759d1b00846e26a39c0f7513fe2ac13d016c3490e70b4d0d20e43</citedby><cites>FETCH-LOGICAL-c640t-e86c2b30e770759d1b00846e26a39c0f7513fe2ac13d016c3490e70b4d0d20e43</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/nrmicro3160$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/nrmicro3160$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,776,780,881,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24384599$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Huang, Ju</creatorcontrib><creatorcontrib>Brumell, John H.</creatorcontrib><title>Bacteria–autophagy interplay: a battle for survival</title><title>Nature reviews. Microbiology</title><addtitle>Nat Rev Microbiol</addtitle><addtitle>Nat Rev Microbiol</addtitle><description>Key Points
Autophagy is used by the cell to degrade various substrates; this is achieved either through the canonical, non-selective autophagy pathway or through selective autophagy. Both pathways proceed via distinct key steps and use specific molecular mechanisms.
The canonical autophagy pathway has been studied in detail in mammalian cells and in model organisms, such as yeast. The molecular mechanisms underlying non-canonical autophagy, in addition to alternative pathways that are independent of some of the key autophagy machinery, are beginning to become clear.
Besides degradation of cellular proteins, autophagy proteins are also involved in many other functions, some of which are important during bacterial infections.
Autophagy functions as an antibacterial mechanism. The induction and recognition mechanisms for several bacterial species have been elucidated.
Bacteria can escape killing by autophagy and some can even use autophagy to promote infection of host cells, through the interaction between bacterial effector proteins and autophagy components.
The knowledge about bacteria–autophagy interactions will inform the design of new drugs and treatments against bacterial infections.
Autophagy not only degrades components of host cells but can also target intracellular bacteria and thus contribute to host defences. Here, Huang and Brumell discuss the canonical and selective pathways of antibacterial autophagy, as well as the ways in which bacteria can escape from them and sometimes even use them to promote infection.
Autophagy is a cellular process that targets proteins, lipids and organelles to lysosomes for degradation, but it has also been shown to combat infection with various pathogenic bacteria. In turn, bacteria have developed diverse strategies to avoid autophagy by interfering with autophagy signalling or the autophagy machinery and, in some cases, they even exploit autophagy for their growth. In this Review, we discuss canonical and non-canonical autophagy pathways and our current knowledge of antibacterial autophagy, with a focus on the interplay between bacterial factors and autophagy components.</description><subject>631/326/41/2531</subject><subject>631/326/41/2533</subject><subject>631/326/41/2534</subject><subject>631/80/39</subject><subject>Antigen presentation</subject><subject>Antiinfectives and antibacterials</subject><subject>Apoptosis</subject><subject>Autophagy</subject><subject>Autophagy (Cytology)</subject><subject>Autophagy - physiology</subject><subject>Bacteria</subject><subject>Bacteria - pathogenicity</subject><subject>Bacterial diseases</subject><subject>Bacterial infections</subject><subject>Biodegradation</subject><subject>Cell cycle</subject><subject>Cell research</subject><subject>Cell survival</subject><subject>Cellular control mechanisms</subject><subject>Cytokines</subject><subject>Drug development</subject><subject>Drug interaction</subject><subject>Effector cells</subject><subject>Host-Pathogen Interactions</subject><subject>Infectious Diseases</subject><subject>Kinases</subject><subject>Life Sciences</subject><subject>Lipids</subject><subject>Lysosomes - metabolism</subject><subject>Lysosomes - microbiology</subject><subject>Mammalian cells</subject><subject>Medical Microbiology</subject><subject>Microbiology</subject><subject>Molecular modelling</subject><subject>Parasitology</subject><subject>Phagocytosis</subject><subject>Phagosomes - metabolism</subject><subject>Phagosomes - microbiology</subject><subject>Physiological aspects</subject><subject>Proteins</subject><subject>Protozoa</subject><subject>review-article</subject><subject>Virology</subject><subject>Yeasts</subject><issn>1740-1526</issn><issn>1740-1534</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqFkk1PGzEQhi3UCijtiTtaqRekNnS8_oo5IAHqBxJSL-3Z8npng9HGTu3dSLn1P_Qf8ktqGhqFChX5YGvm8Tue8UvIIYUTCmz6IaS5dykyKmGH7FPFYUIF4y8251rukVc53wLUQqh6l-zVnE250HqfiAvrBkze3v38ZcchLm7sbFX5UGKL3q5OK1s1dhh6rLqYqjympV_a_jV52dk-45uH_YB8__Tx2-WXyfXXz1eX59cTJzkME5xKVzcMUClQQre0AZhyibW0TDvolKCsw9o6ylqg0jGuCwsNb6GtATk7IGdr3cXYzLF1GIZke7NIfm7TykTrzeNM8DdmFpdGgVZcqSJw_CCQ4o8R82DmPjvsexswjtlQAWVUQBl7Hi2PUxKEpgV9-w96G8cUyiQMo5yB1ozz_1FUSuBSiG1qZns0PnSxNOLuS5tzJrSkgv6pePIEVVaL5fNjwM6X-KML79YXijNyTththkbB3NvGbNmm0Efbc96wf31SgPdrIJdUmGHa6uUJvd8wD8tV</recordid><startdate>20140201</startdate><enddate>20140201</enddate><creator>Huang, Ju</creator><creator>Brumell, John H.</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</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>7RV</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</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>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>BKSAR</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>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7N</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>P64</scope><scope>PCBAR</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>RC3</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20140201</creationdate><title>Bacteria–autophagy interplay: a battle for survival</title><author>Huang, Ju ; Brumell, John H.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c640t-e86c2b30e770759d1b00846e26a39c0f7513fe2ac13d016c3490e70b4d0d20e43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>631/326/41/2531</topic><topic>631/326/41/2533</topic><topic>631/326/41/2534</topic><topic>631/80/39</topic><topic>Antigen presentation</topic><topic>Antiinfectives and antibacterials</topic><topic>Apoptosis</topic><topic>Autophagy</topic><topic>Autophagy (Cytology)</topic><topic>Autophagy - physiology</topic><topic>Bacteria</topic><topic>Bacteria - pathogenicity</topic><topic>Bacterial diseases</topic><topic>Bacterial infections</topic><topic>Biodegradation</topic><topic>Cell cycle</topic><topic>Cell research</topic><topic>Cell survival</topic><topic>Cellular control mechanisms</topic><topic>Cytokines</topic><topic>Drug development</topic><topic>Drug interaction</topic><topic>Effector cells</topic><topic>Host-Pathogen Interactions</topic><topic>Infectious Diseases</topic><topic>Kinases</topic><topic>Life Sciences</topic><topic>Lipids</topic><topic>Lysosomes - metabolism</topic><topic>Lysosomes - microbiology</topic><topic>Mammalian cells</topic><topic>Medical Microbiology</topic><topic>Microbiology</topic><topic>Molecular modelling</topic><topic>Parasitology</topic><topic>Phagocytosis</topic><topic>Phagosomes - metabolism</topic><topic>Phagosomes - microbiology</topic><topic>Physiological aspects</topic><topic>Proteins</topic><topic>Protozoa</topic><topic>review-article</topic><topic>Virology</topic><topic>Yeasts</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Huang, Ju</creatorcontrib><creatorcontrib>Brumell, John 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>Nursing & Allied Health Database</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science 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 Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>Earth, Atmospheric & Aquatic Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</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>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Earth, Atmospheric & Aquatic Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Nature reviews. Microbiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Huang, Ju</au><au>Brumell, John H.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Bacteria–autophagy interplay: a battle for survival</atitle><jtitle>Nature reviews. Microbiology</jtitle><stitle>Nat Rev Microbiol</stitle><addtitle>Nat Rev Microbiol</addtitle><date>2014-02-01</date><risdate>2014</risdate><volume>12</volume><issue>2</issue><spage>101</spage><epage>114</epage><pages>101-114</pages><issn>1740-1526</issn><eissn>1740-1534</eissn><abstract>Key Points
Autophagy is used by the cell to degrade various substrates; this is achieved either through the canonical, non-selective autophagy pathway or through selective autophagy. Both pathways proceed via distinct key steps and use specific molecular mechanisms.
The canonical autophagy pathway has been studied in detail in mammalian cells and in model organisms, such as yeast. The molecular mechanisms underlying non-canonical autophagy, in addition to alternative pathways that are independent of some of the key autophagy machinery, are beginning to become clear.
Besides degradation of cellular proteins, autophagy proteins are also involved in many other functions, some of which are important during bacterial infections.
Autophagy functions as an antibacterial mechanism. The induction and recognition mechanisms for several bacterial species have been elucidated.
Bacteria can escape killing by autophagy and some can even use autophagy to promote infection of host cells, through the interaction between bacterial effector proteins and autophagy components.
The knowledge about bacteria–autophagy interactions will inform the design of new drugs and treatments against bacterial infections.
Autophagy not only degrades components of host cells but can also target intracellular bacteria and thus contribute to host defences. Here, Huang and Brumell discuss the canonical and selective pathways of antibacterial autophagy, as well as the ways in which bacteria can escape from them and sometimes even use them to promote infection.
Autophagy is a cellular process that targets proteins, lipids and organelles to lysosomes for degradation, but it has also been shown to combat infection with various pathogenic bacteria. In turn, bacteria have developed diverse strategies to avoid autophagy by interfering with autophagy signalling or the autophagy machinery and, in some cases, they even exploit autophagy for their growth. In this Review, we discuss canonical and non-canonical autophagy pathways and our current knowledge of antibacterial autophagy, with a focus on the interplay between bacterial factors and autophagy components.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>24384599</pmid><doi>10.1038/nrmicro3160</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record> |
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subjects | 631/326/41/2531 631/326/41/2533 631/326/41/2534 631/80/39 Antigen presentation Antiinfectives and antibacterials Apoptosis Autophagy Autophagy (Cytology) Autophagy - physiology Bacteria Bacteria - pathogenicity Bacterial diseases Bacterial infections Biodegradation Cell cycle Cell research Cell survival Cellular control mechanisms Cytokines Drug development Drug interaction Effector cells Host-Pathogen Interactions Infectious Diseases Kinases Life Sciences Lipids Lysosomes - metabolism Lysosomes - microbiology Mammalian cells Medical Microbiology Microbiology Molecular modelling Parasitology Phagocytosis Phagosomes - metabolism Phagosomes - microbiology Physiological aspects Proteins Protozoa review-article Virology Yeasts |
title | Bacteria–autophagy interplay: a battle for survival |
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