CASP4/caspase-11 promotes autophagosome formation in response to bacterial infection
CASP4/caspase-11-dependent inflammasome activation is important for the clearance of various Gram-negative bacteria entering the host cytosol. Additionally, CASP4 modulates the actin cytoskeleton to promote the maturation of phagosomes harboring intracellular pathogens such as Legionella pneumophila...
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| Veröffentlicht in: | Autophagy 2018-11, Vol.14 (11), p.1928-1942 |
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| container_title | Autophagy |
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| creator | Krause, Kathrin Caution, Kyle Badr, Asmaa Hamilton, Kaitlin Saleh, Abdulmuti Patel, Khushbu Seveau, Stephanie Hall-Stoodley, Luanne Hegazi, Rana Zhang, Xiaoli Gavrilin, Mikhail A. Amer, Amal O. |
| description | CASP4/caspase-11-dependent inflammasome activation is important for the clearance of various Gram-negative bacteria entering the host cytosol. Additionally, CASP4 modulates the actin cytoskeleton to promote the maturation of phagosomes harboring intracellular pathogens such as Legionella pneumophila but not those enclosing nonpathogenic bacteria. Nevertheless, this non-inflammatory role of CASP4 regarding the trafficking of vacuolar bacteria remains poorly understood. Macroautophagy/autophagy, a catabolic process within eukaryotic cells, is also implicated in the elimination of intracellular pathogens such as Burkholderia cenocepacia. Here we show that CASP4-deficient macrophages exhibit a defect in autophagosome formation in response to B. cenocepacia infection. The absence of CASP4 causes an accumulation of the small GTPase RAB7, reduced colocalization of B. cenocepacia with LC3 and acidic compartments accompanied by increased bacterial replication in vitro and in vivo. Together, our data reveal a novel role of CASP4 in regulating autophagy in response to B. cenocepacia infection. |
| doi_str_mv | 10.1080/15548627.2018.1491494 |
| format | Article |
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Additionally, CASP4 modulates the actin cytoskeleton to promote the maturation of phagosomes harboring intracellular pathogens such as Legionella pneumophila but not those enclosing nonpathogenic bacteria. Nevertheless, this non-inflammatory role of CASP4 regarding the trafficking of vacuolar bacteria remains poorly understood. Macroautophagy/autophagy, a catabolic process within eukaryotic cells, is also implicated in the elimination of intracellular pathogens such as Burkholderia cenocepacia. Here we show that CASP4-deficient macrophages exhibit a defect in autophagosome formation in response to B. cenocepacia infection. The absence of CASP4 causes an accumulation of the small GTPase RAB7, reduced colocalization of B. cenocepacia with LC3 and acidic compartments accompanied by increased bacterial replication in vitro and in vivo. Together, our data reveal a novel role of CASP4 in regulating autophagy in response to B. cenocepacia infection.</description><identifier>ISSN: 1554-8627</identifier><identifier>EISSN: 1554-8635</identifier><identifier>DOI: 10.1080/15548627.2018.1491494</identifier><identifier>PMID: 30165781</identifier><language>eng</language><publisher>United States: Taylor & Francis</publisher><subject>Animals ; Autophagosomes - metabolism ; Autophagosomes - microbiology ; autophagy ; Autophagy - genetics ; Autophagy - immunology ; Bacterial Infections - genetics ; Bacterial Infections - immunology ; Bacterial Infections - metabolism ; Burkholderia cenocepacia ; Burkholderia cenocepacia - immunology ; Burkholderia cenocepacia - metabolism ; Burkholderia Infections - genetics ; Burkholderia Infections - immunology ; Burkholderia Infections - metabolism ; caspase-1 (CASP1) ; caspase-11 (CASP4) ; Caspases - genetics ; Caspases - physiology ; Cells, Cultured ; Escherichia coli - immunology ; Escherichia coli - metabolism ; Inflammasomes - genetics ; Inflammasomes - metabolism ; lysosome ; macrophages ; Macrophages - immunology ; Macrophages - metabolism ; Macrophages - microbiology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Phagosomes - genetics ; Phagosomes - metabolism ; Phagosomes - microbiology ; Phagosomes - pathology ; Research Paper - Basic Science</subject><ispartof>Autophagy, 2018-11, Vol.14 (11), p.1928-1942</ispartof><rights>2018 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. 2018</rights><rights>2018 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. 2018 The Author(s)</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c468t-e7838b067f427a8ce98f5f4adc08c8c40069bc79e0447b929f291a4ab2472983</citedby><cites>FETCH-LOGICAL-c468t-e7838b067f427a8ce98f5f4adc08c8c40069bc79e0447b929f291a4ab2472983</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6152495/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6152495/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30165781$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Krause, Kathrin</creatorcontrib><creatorcontrib>Caution, Kyle</creatorcontrib><creatorcontrib>Badr, Asmaa</creatorcontrib><creatorcontrib>Hamilton, Kaitlin</creatorcontrib><creatorcontrib>Saleh, Abdulmuti</creatorcontrib><creatorcontrib>Patel, Khushbu</creatorcontrib><creatorcontrib>Seveau, Stephanie</creatorcontrib><creatorcontrib>Hall-Stoodley, Luanne</creatorcontrib><creatorcontrib>Hegazi, Rana</creatorcontrib><creatorcontrib>Zhang, Xiaoli</creatorcontrib><creatorcontrib>Gavrilin, Mikhail A.</creatorcontrib><creatorcontrib>Amer, Amal O.</creatorcontrib><title>CASP4/caspase-11 promotes autophagosome formation in response to bacterial infection</title><title>Autophagy</title><addtitle>Autophagy</addtitle><description>CASP4/caspase-11-dependent inflammasome activation is important for the clearance of various Gram-negative bacteria entering the host cytosol. Additionally, CASP4 modulates the actin cytoskeleton to promote the maturation of phagosomes harboring intracellular pathogens such as Legionella pneumophila but not those enclosing nonpathogenic bacteria. Nevertheless, this non-inflammatory role of CASP4 regarding the trafficking of vacuolar bacteria remains poorly understood. Macroautophagy/autophagy, a catabolic process within eukaryotic cells, is also implicated in the elimination of intracellular pathogens such as Burkholderia cenocepacia. Here we show that CASP4-deficient macrophages exhibit a defect in autophagosome formation in response to B. cenocepacia infection. The absence of CASP4 causes an accumulation of the small GTPase RAB7, reduced colocalization of B. cenocepacia with LC3 and acidic compartments accompanied by increased bacterial replication in vitro and in vivo. Together, our data reveal a novel role of CASP4 in regulating autophagy in response to B. cenocepacia infection.</description><subject>Animals</subject><subject>Autophagosomes - metabolism</subject><subject>Autophagosomes - microbiology</subject><subject>autophagy</subject><subject>Autophagy - genetics</subject><subject>Autophagy - immunology</subject><subject>Bacterial Infections - genetics</subject><subject>Bacterial Infections - immunology</subject><subject>Bacterial Infections - metabolism</subject><subject>Burkholderia cenocepacia</subject><subject>Burkholderia cenocepacia - immunology</subject><subject>Burkholderia cenocepacia - metabolism</subject><subject>Burkholderia Infections - genetics</subject><subject>Burkholderia Infections - immunology</subject><subject>Burkholderia Infections - metabolism</subject><subject>caspase-1 (CASP1)</subject><subject>caspase-11 (CASP4)</subject><subject>Caspases - genetics</subject><subject>Caspases - physiology</subject><subject>Cells, Cultured</subject><subject>Escherichia coli - immunology</subject><subject>Escherichia coli - metabolism</subject><subject>Inflammasomes - genetics</subject><subject>Inflammasomes - metabolism</subject><subject>lysosome</subject><subject>macrophages</subject><subject>Macrophages - immunology</subject><subject>Macrophages - metabolism</subject><subject>Macrophages - microbiology</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Phagosomes - genetics</subject><subject>Phagosomes - metabolism</subject><subject>Phagosomes - microbiology</subject><subject>Phagosomes - pathology</subject><subject>Research Paper - Basic Science</subject><issn>1554-8627</issn><issn>1554-8635</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>0YH</sourceid><sourceid>EIF</sourceid><recordid>eNp9kVtr3DAQhUVJadK0P6HBj3nxRpJ1fQkJS28QaKH7LsbaUeJgW66kTci_r81ulvalIJCYOXOOmI-QT4yuGDX0ikkpjOJ6xSkzKybsfMQbcrbUa6MaeXJ8c31K3uf8SGmjjOXvyGlDmZLasDOyWd_--imuPOQJMtaMVVOKQyyYK9iVOD3AfcxxwCrENEDp4lh1Y5UwT3HMWJVYteALpg76uRHQL5IP5G2APuPHw31ONl8-b9bf6rsfX7-vb-9qL5QpNWrTmJYqHQTXYDxaE2QQsPXUeOMFpcq2XlukQujWchu4ZSCg5UJza5pzcr23nXbtgFuPY0nQuyl1A6QXF6Fz_3bG7sHdxyenmOTCytng8mCQ4u8d5uKGLnvsexgx7rLj1BqtJJNLltxLfYo5JwzHGEbdAsS9AnELEHcAMs9d_P3H49QrgVlwsxfM21tW_BxTv3UFXvqYQoLRd9k1_8_4A_tOm5k</recordid><startdate>20181102</startdate><enddate>20181102</enddate><creator>Krause, Kathrin</creator><creator>Caution, Kyle</creator><creator>Badr, Asmaa</creator><creator>Hamilton, Kaitlin</creator><creator>Saleh, Abdulmuti</creator><creator>Patel, Khushbu</creator><creator>Seveau, Stephanie</creator><creator>Hall-Stoodley, Luanne</creator><creator>Hegazi, Rana</creator><creator>Zhang, Xiaoli</creator><creator>Gavrilin, Mikhail A.</creator><creator>Amer, Amal O.</creator><general>Taylor & Francis</general><scope>0YH</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>7X8</scope><scope>5PM</scope></search><sort><creationdate>20181102</creationdate><title>CASP4/caspase-11 promotes autophagosome formation in response to bacterial infection</title><author>Krause, Kathrin ; Caution, Kyle ; Badr, Asmaa ; Hamilton, Kaitlin ; Saleh, Abdulmuti ; Patel, Khushbu ; Seveau, Stephanie ; Hall-Stoodley, Luanne ; Hegazi, Rana ; Zhang, Xiaoli ; Gavrilin, Mikhail A. ; Amer, Amal O.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c468t-e7838b067f427a8ce98f5f4adc08c8c40069bc79e0447b929f291a4ab2472983</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Animals</topic><topic>Autophagosomes - metabolism</topic><topic>Autophagosomes - microbiology</topic><topic>autophagy</topic><topic>Autophagy - genetics</topic><topic>Autophagy - immunology</topic><topic>Bacterial Infections - genetics</topic><topic>Bacterial Infections - immunology</topic><topic>Bacterial Infections - metabolism</topic><topic>Burkholderia cenocepacia</topic><topic>Burkholderia cenocepacia - immunology</topic><topic>Burkholderia cenocepacia - metabolism</topic><topic>Burkholderia Infections - genetics</topic><topic>Burkholderia Infections - immunology</topic><topic>Burkholderia Infections - metabolism</topic><topic>caspase-1 (CASP1)</topic><topic>caspase-11 (CASP4)</topic><topic>Caspases - genetics</topic><topic>Caspases - physiology</topic><topic>Cells, Cultured</topic><topic>Escherichia coli - immunology</topic><topic>Escherichia coli - metabolism</topic><topic>Inflammasomes - genetics</topic><topic>Inflammasomes - metabolism</topic><topic>lysosome</topic><topic>macrophages</topic><topic>Macrophages - immunology</topic><topic>Macrophages - metabolism</topic><topic>Macrophages - microbiology</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Phagosomes - genetics</topic><topic>Phagosomes - metabolism</topic><topic>Phagosomes - microbiology</topic><topic>Phagosomes - pathology</topic><topic>Research Paper - Basic Science</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Krause, Kathrin</creatorcontrib><creatorcontrib>Caution, Kyle</creatorcontrib><creatorcontrib>Badr, Asmaa</creatorcontrib><creatorcontrib>Hamilton, Kaitlin</creatorcontrib><creatorcontrib>Saleh, Abdulmuti</creatorcontrib><creatorcontrib>Patel, Khushbu</creatorcontrib><creatorcontrib>Seveau, Stephanie</creatorcontrib><creatorcontrib>Hall-Stoodley, Luanne</creatorcontrib><creatorcontrib>Hegazi, Rana</creatorcontrib><creatorcontrib>Zhang, Xiaoli</creatorcontrib><creatorcontrib>Gavrilin, Mikhail A.</creatorcontrib><creatorcontrib>Amer, Amal O.</creatorcontrib><collection>Taylor & Francis Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Autophagy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Krause, Kathrin</au><au>Caution, Kyle</au><au>Badr, Asmaa</au><au>Hamilton, Kaitlin</au><au>Saleh, Abdulmuti</au><au>Patel, Khushbu</au><au>Seveau, Stephanie</au><au>Hall-Stoodley, Luanne</au><au>Hegazi, Rana</au><au>Zhang, Xiaoli</au><au>Gavrilin, Mikhail A.</au><au>Amer, Amal O.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CASP4/caspase-11 promotes autophagosome formation in response to bacterial infection</atitle><jtitle>Autophagy</jtitle><addtitle>Autophagy</addtitle><date>2018-11-02</date><risdate>2018</risdate><volume>14</volume><issue>11</issue><spage>1928</spage><epage>1942</epage><pages>1928-1942</pages><issn>1554-8627</issn><eissn>1554-8635</eissn><abstract>CASP4/caspase-11-dependent inflammasome activation is important for the clearance of various Gram-negative bacteria entering the host cytosol. Additionally, CASP4 modulates the actin cytoskeleton to promote the maturation of phagosomes harboring intracellular pathogens such as Legionella pneumophila but not those enclosing nonpathogenic bacteria. Nevertheless, this non-inflammatory role of CASP4 regarding the trafficking of vacuolar bacteria remains poorly understood. Macroautophagy/autophagy, a catabolic process within eukaryotic cells, is also implicated in the elimination of intracellular pathogens such as Burkholderia cenocepacia. Here we show that CASP4-deficient macrophages exhibit a defect in autophagosome formation in response to B. cenocepacia infection. The absence of CASP4 causes an accumulation of the small GTPase RAB7, reduced colocalization of B. cenocepacia with LC3 and acidic compartments accompanied by increased bacterial replication in vitro and in vivo. Together, our data reveal a novel role of CASP4 in regulating autophagy in response to B. cenocepacia infection.</abstract><cop>United States</cop><pub>Taylor & Francis</pub><pmid>30165781</pmid><doi>10.1080/15548627.2018.1491494</doi><tpages>15</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Autophagosomes - metabolism Autophagosomes - microbiology autophagy Autophagy - genetics Autophagy - immunology Bacterial Infections - genetics Bacterial Infections - immunology Bacterial Infections - metabolism Burkholderia cenocepacia Burkholderia cenocepacia - immunology Burkholderia cenocepacia - metabolism Burkholderia Infections - genetics Burkholderia Infections - immunology Burkholderia Infections - metabolism caspase-1 (CASP1) caspase-11 (CASP4) Caspases - genetics Caspases - physiology Cells, Cultured Escherichia coli - immunology Escherichia coli - metabolism Inflammasomes - genetics Inflammasomes - metabolism lysosome macrophages Macrophages - immunology Macrophages - metabolism Macrophages - microbiology Mice Mice, Inbred C57BL Mice, Knockout Phagosomes - genetics Phagosomes - metabolism Phagosomes - microbiology Phagosomes - pathology Research Paper - Basic Science |
| title | CASP4/caspase-11 promotes autophagosome formation in response to bacterial infection |
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