Revealing the Mechanism of NLRP3 Inflammatory Pathway Activation through K + Efflux Induced by PLO via Signal Point Mutations
is an important opportunistic pathogenic bacterium widely distributed in the environment. Pyolysin (PLO) is a primary virulence factor of and capable of lysing many different cells. PLO is a member of the cholesterol-dependent cytolysin (CDC) family of which the primary structure only presents a low...
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| Veröffentlicht in: | International journal of molecular sciences 2024-06, Vol.25 (12), p.6703 |
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| creator | Shan, Qiang Ma, Wenbo Li, Bolin Li, Qian Wang, Xue Li, Yanan Wang, Jiufeng Zhu, Yaohong Liu, Ning |
| description | is an important opportunistic pathogenic bacterium widely distributed in the environment. Pyolysin (PLO) is a primary virulence factor of
and capable of lysing many different cells. PLO is a member of the cholesterol-dependent cytolysin (CDC) family of which the primary structure only presents a low level of homology with other members from 31% to 45%. By deeply studying PLO, we can understand the overall pathogenic mechanism of CDC family proteins. This study established a mouse muscle tissue model infected with recombinant PLO (rPLO) and its single-point mutations, rPLO N139K and rPLO F240A, and explored its mechanism of causing inflammatory damage. The inflammatory injury abilities of rPLO N139K and rPLO F240A are significantly reduced compared to rPLO. This study elaborated on the inflammatory mechanism of PLO by examining its unit point mutations in detail. Our data also provide a theoretical basis and practical significance for future research on toxins and bacteria. |
| doi_str_mv | 10.3390/ijms25126703 |
| format | Article |
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and capable of lysing many different cells. PLO is a member of the cholesterol-dependent cytolysin (CDC) family of which the primary structure only presents a low level of homology with other members from 31% to 45%. By deeply studying PLO, we can understand the overall pathogenic mechanism of CDC family proteins. This study established a mouse muscle tissue model infected with recombinant PLO (rPLO) and its single-point mutations, rPLO N139K and rPLO F240A, and explored its mechanism of causing inflammatory damage. The inflammatory injury abilities of rPLO N139K and rPLO F240A are significantly reduced compared to rPLO. This study elaborated on the inflammatory mechanism of PLO by examining its unit point mutations in detail. Our data also provide a theoretical basis and practical significance for future research on toxins and bacteria.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms25126703</identifier><identifier>PMID: 38928408</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>Analysis ; Animals ; Bacteria ; Bacterial Proteins - genetics ; Bacterial Proteins - metabolism ; Bacterial Toxins - genetics ; Bacterial Toxins - metabolism ; Gene mutations ; Genes ; Genetic aspects ; Hemolysin Proteins - genetics ; Hemolysin Proteins - metabolism ; Humans ; Inflammasomes - metabolism ; Inflammation - genetics ; Inflammation - metabolism ; Inflammatory diseases ; Mice ; Mutation ; NLR Family, Pyrin Domain-Containing 3 Protein - genetics ; NLR Family, Pyrin Domain-Containing 3 Protein - metabolism ; Point Mutation ; Potassium ; Potassium - metabolism ; Proteins ; Signal Transduction ; Toxins ; Virulence</subject><ispartof>International journal of molecular sciences, 2024-06, Vol.25 (12), p.6703</ispartof><rights>COPYRIGHT 2024 MDPI AG</rights><rights>2024 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2024 by the authors. 2024</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c339t-d0088bb27129e800ed69364bf01e10f72328417344968e8be7c7aafb32263de63</cites><orcidid>0000-0002-0183-5611</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11203744/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11203744/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38928408$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shan, Qiang</creatorcontrib><creatorcontrib>Ma, Wenbo</creatorcontrib><creatorcontrib>Li, Bolin</creatorcontrib><creatorcontrib>Li, Qian</creatorcontrib><creatorcontrib>Wang, Xue</creatorcontrib><creatorcontrib>Li, Yanan</creatorcontrib><creatorcontrib>Wang, Jiufeng</creatorcontrib><creatorcontrib>Zhu, Yaohong</creatorcontrib><creatorcontrib>Liu, Ning</creatorcontrib><title>Revealing the Mechanism of NLRP3 Inflammatory Pathway Activation through K + Efflux Induced by PLO via Signal Point Mutations</title><title>International journal of molecular sciences</title><addtitle>Int J Mol Sci</addtitle><description>is an important opportunistic pathogenic bacterium widely distributed in the environment. Pyolysin (PLO) is a primary virulence factor of
and capable of lysing many different cells. PLO is a member of the cholesterol-dependent cytolysin (CDC) family of which the primary structure only presents a low level of homology with other members from 31% to 45%. By deeply studying PLO, we can understand the overall pathogenic mechanism of CDC family proteins. This study established a mouse muscle tissue model infected with recombinant PLO (rPLO) and its single-point mutations, rPLO N139K and rPLO F240A, and explored its mechanism of causing inflammatory damage. The inflammatory injury abilities of rPLO N139K and rPLO F240A are significantly reduced compared to rPLO. This study elaborated on the inflammatory mechanism of PLO by examining its unit point mutations in detail. Our data also provide a theoretical basis and practical significance for future research on toxins and bacteria.</description><subject>Analysis</subject><subject>Animals</subject><subject>Bacteria</subject><subject>Bacterial Proteins - genetics</subject><subject>Bacterial Proteins - metabolism</subject><subject>Bacterial Toxins - genetics</subject><subject>Bacterial Toxins - metabolism</subject><subject>Gene mutations</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Hemolysin Proteins - genetics</subject><subject>Hemolysin Proteins - metabolism</subject><subject>Humans</subject><subject>Inflammasomes - metabolism</subject><subject>Inflammation - genetics</subject><subject>Inflammation - metabolism</subject><subject>Inflammatory diseases</subject><subject>Mice</subject><subject>Mutation</subject><subject>NLR Family, Pyrin Domain-Containing 3 Protein - genetics</subject><subject>NLR Family, Pyrin Domain-Containing 3 Protein - metabolism</subject><subject>Point Mutation</subject><subject>Potassium</subject><subject>Potassium - metabolism</subject><subject>Proteins</subject><subject>Signal Transduction</subject><subject>Toxins</subject><subject>Virulence</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpdks1vFCEYxidGY2v15tmQeDGxW_nagTk1m6bWxq3dVD0ThnmZYTMDdWBW9-D_Lu3WZjUcIPB7npcH3qJ4TfAJYxX-4NZDpHNCS4HZk-KQcEpnGJfi6d76oHgR4xpjyui8el4cMFlRybE8LH7fwAZ073yLUgfoCkynvYsDChZ9Wd6sGLr0ttfDoFMYt2ilU_dTb9HCJLfRyQWfZWOY2g59Ru_RubX99CtLmslAg-osWF6jjdPoq2u97tEqOJ_Q1ZTutfFl8czqPsKrh_mo-P7x_NvZp9ny-uLybLGcmRwxzRqMpaxrKgitQGIMTVmxktcWEyDYihxLciIY51UpQdYgjNDa1ozSkjVQsqPidOd7O9UDNAZ8GnWvbkc36HGrgnbq3xPvOtWGjSKEYiY4zw7vHhzG8GOCmNTgooG-1x7CFBXDgkrM8_tm9O1_6DpMY06_o9icl0xk6mRHtboH5bwNubDJo4HBmeDBury_EFVVcornVRYc7wRmDDGOYB-vT7C66wS13wkZf7Mf-RH--_XsD0GRrik</recordid><startdate>20240618</startdate><enddate>20240618</enddate><creator>Shan, Qiang</creator><creator>Ma, Wenbo</creator><creator>Li, Bolin</creator><creator>Li, Qian</creator><creator>Wang, Xue</creator><creator>Li, Yanan</creator><creator>Wang, Jiufeng</creator><creator>Zhu, Yaohong</creator><creator>Liu, Ning</creator><general>MDPI AG</general><general>MDPI</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>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-0183-5611</orcidid></search><sort><creationdate>20240618</creationdate><title>Revealing the Mechanism of NLRP3 Inflammatory Pathway Activation through K + Efflux Induced by PLO via Signal Point Mutations</title><author>Shan, Qiang ; Ma, Wenbo ; Li, Bolin ; Li, Qian ; Wang, Xue ; Li, Yanan ; Wang, Jiufeng ; Zhu, Yaohong ; Liu, Ning</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c339t-d0088bb27129e800ed69364bf01e10f72328417344968e8be7c7aafb32263de63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Analysis</topic><topic>Animals</topic><topic>Bacteria</topic><topic>Bacterial Proteins - genetics</topic><topic>Bacterial Proteins - metabolism</topic><topic>Bacterial Toxins - genetics</topic><topic>Bacterial Toxins - metabolism</topic><topic>Gene mutations</topic><topic>Genes</topic><topic>Genetic aspects</topic><topic>Hemolysin Proteins - genetics</topic><topic>Hemolysin Proteins - metabolism</topic><topic>Humans</topic><topic>Inflammasomes - metabolism</topic><topic>Inflammation - genetics</topic><topic>Inflammation - metabolism</topic><topic>Inflammatory diseases</topic><topic>Mice</topic><topic>Mutation</topic><topic>NLR Family, Pyrin Domain-Containing 3 Protein - genetics</topic><topic>NLR Family, Pyrin Domain-Containing 3 Protein - metabolism</topic><topic>Point Mutation</topic><topic>Potassium</topic><topic>Potassium - metabolism</topic><topic>Proteins</topic><topic>Signal Transduction</topic><topic>Toxins</topic><topic>Virulence</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shan, Qiang</creatorcontrib><creatorcontrib>Ma, Wenbo</creatorcontrib><creatorcontrib>Li, Bolin</creatorcontrib><creatorcontrib>Li, Qian</creatorcontrib><creatorcontrib>Wang, Xue</creatorcontrib><creatorcontrib>Li, Yanan</creatorcontrib><creatorcontrib>Wang, Jiufeng</creatorcontrib><creatorcontrib>Zhu, Yaohong</creatorcontrib><creatorcontrib>Liu, Ning</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>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content 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 China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>International journal of molecular sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shan, Qiang</au><au>Ma, Wenbo</au><au>Li, Bolin</au><au>Li, Qian</au><au>Wang, Xue</au><au>Li, Yanan</au><au>Wang, Jiufeng</au><au>Zhu, Yaohong</au><au>Liu, Ning</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Revealing the Mechanism of NLRP3 Inflammatory Pathway Activation through K + Efflux Induced by PLO via Signal Point Mutations</atitle><jtitle>International journal of molecular sciences</jtitle><addtitle>Int J Mol Sci</addtitle><date>2024-06-18</date><risdate>2024</risdate><volume>25</volume><issue>12</issue><spage>6703</spage><pages>6703-</pages><issn>1422-0067</issn><issn>1661-6596</issn><eissn>1422-0067</eissn><abstract>is an important opportunistic pathogenic bacterium widely distributed in the environment. Pyolysin (PLO) is a primary virulence factor of
and capable of lysing many different cells. PLO is a member of the cholesterol-dependent cytolysin (CDC) family of which the primary structure only presents a low level of homology with other members from 31% to 45%. By deeply studying PLO, we can understand the overall pathogenic mechanism of CDC family proteins. This study established a mouse muscle tissue model infected with recombinant PLO (rPLO) and its single-point mutations, rPLO N139K and rPLO F240A, and explored its mechanism of causing inflammatory damage. The inflammatory injury abilities of rPLO N139K and rPLO F240A are significantly reduced compared to rPLO. This study elaborated on the inflammatory mechanism of PLO by examining its unit point mutations in detail. Our data also provide a theoretical basis and practical significance for future research on toxins and bacteria.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>38928408</pmid><doi>10.3390/ijms25126703</doi><orcidid>https://orcid.org/0000-0002-0183-5611</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Analysis Animals Bacteria Bacterial Proteins - genetics Bacterial Proteins - metabolism Bacterial Toxins - genetics Bacterial Toxins - metabolism Gene mutations Genes Genetic aspects Hemolysin Proteins - genetics Hemolysin Proteins - metabolism Humans Inflammasomes - metabolism Inflammation - genetics Inflammation - metabolism Inflammatory diseases Mice Mutation NLR Family, Pyrin Domain-Containing 3 Protein - genetics NLR Family, Pyrin Domain-Containing 3 Protein - metabolism Point Mutation Potassium Potassium - metabolism Proteins Signal Transduction Toxins Virulence |
| title | Revealing the Mechanism of NLRP3 Inflammatory Pathway Activation through K + Efflux Induced by PLO via Signal Point Mutations |
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