Antimicrobial peptide HPA3NT3-A2 effectively inhibits biofilm formation in mice infected with drug-resistant bacteria
Bacterial biofilms formed through secretion of extracellular polymeric substances (EPS) have been implicated in many serious infections and can increase antibiotic resistance by a factor of more than 1000. Here, we examined the abilities of the antimicrobial peptide HPA3NT3-A2 to inhibit and reduce...
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| Veröffentlicht in: | Biomaterials science 2019-11, Vol.7 (12), p.568-583 |
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| creator | Lee, Jong-Kook Mereuta, Loredana Luchian, Tudor Park, Yoonkyung |
| description | Bacterial biofilms formed through secretion of extracellular polymeric substances (EPS) have been implicated in many serious infections and can increase antibiotic resistance by a factor of more than 1000. Here, we examined the abilities of the antimicrobial peptide HPA3NT3-A2 to inhibit and reduce biofilm formation, eliminate EPS, and suppress inflammation in mice infected with clinical isolates of drug-resistant
Pseudomonas aeruginosa
strains. HPA3NT3-A2 was developed from a desirable analogue peptide, HPA3NT3, derived from residues 2-20 of the
Helicobacter pylori
ribosomal protein L1. HPA3NT3-A2 showed stronger activity against planktonic cells (MIC: 8 μM) compared to ciprofloxacin or tobramycin (>512 μM), and a favorable minimum biofilm inhibition and elimination concentration. This peptide also neutralized LPS; decreased levels of EPS; inhibited the production of pro-inflammatory cytokines in the lung, kidney, and spleen; decreased white blood cell counts; and increased survival among infected mice.
Bacterial biofilms formed through secretion of extracellular polymeric substances (EPS) have been implicated in many serious infections and can increase antibiotic resistance by a factor of more than 1000. |
| doi_str_mv | 10.1039/c9bm01051c |
| format | Article |
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Pseudomonas aeruginosa
strains. HPA3NT3-A2 was developed from a desirable analogue peptide, HPA3NT3, derived from residues 2-20 of the
Helicobacter pylori
ribosomal protein L1. HPA3NT3-A2 showed stronger activity against planktonic cells (MIC: 8 μM) compared to ciprofloxacin or tobramycin (>512 μM), and a favorable minimum biofilm inhibition and elimination concentration. This peptide also neutralized LPS; decreased levels of EPS; inhibited the production of pro-inflammatory cytokines in the lung, kidney, and spleen; decreased white blood cell counts; and increased survival among infected mice.
Bacterial biofilms formed through secretion of extracellular polymeric substances (EPS) have been implicated in many serious infections and can increase antibiotic resistance by a factor of more than 1000.</description><identifier>ISSN: 2047-4830</identifier><identifier>EISSN: 2047-4849</identifier><identifier>DOI: 10.1039/c9bm01051c</identifier><identifier>PMID: 31555777</identifier><language>eng</language><publisher>England: Royal Society of Chemistry</publisher><subject>Animals ; Antibiotics ; Antiinfectives and antibacterials ; Antimicrobial Cationic Peptides - pharmacology ; Biofilms ; Biofilms - drug effects ; Biofilms - growth & development ; Cytokines ; Drug resistance ; Drug Resistance, Bacterial - drug effects ; Extracellular Polymeric Substance Matrix - metabolism ; Guinea Pigs ; Leukocytes ; Lipopolysaccharides - metabolism ; Mice ; Microbial Sensitivity Tests ; Peptide Fragments - pharmacology ; Peptides ; Pseudomonas aeruginosa ; Pseudomonas aeruginosa - cytology ; Pseudomonas aeruginosa - drug effects ; Pseudomonas aeruginosa - physiology ; Resistance factors ; Ribosomal Proteins - chemistry ; Secretions ; Spleen</subject><ispartof>Biomaterials science, 2019-11, Vol.7 (12), p.568-583</ispartof><rights>Copyright Royal Society of Chemistry 2019</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c404t-333269a6987437813e0b60396db339b4994086b0cdcbf457db17994866f3a0af3</citedby><cites>FETCH-LOGICAL-c404t-333269a6987437813e0b60396db339b4994086b0cdcbf457db17994866f3a0af3</cites><orcidid>0000-0002-8717-3080</orcidid></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/31555777$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lee, Jong-Kook</creatorcontrib><creatorcontrib>Mereuta, Loredana</creatorcontrib><creatorcontrib>Luchian, Tudor</creatorcontrib><creatorcontrib>Park, Yoonkyung</creatorcontrib><title>Antimicrobial peptide HPA3NT3-A2 effectively inhibits biofilm formation in mice infected with drug-resistant bacteria</title><title>Biomaterials science</title><addtitle>Biomater Sci</addtitle><description>Bacterial biofilms formed through secretion of extracellular polymeric substances (EPS) have been implicated in many serious infections and can increase antibiotic resistance by a factor of more than 1000. Here, we examined the abilities of the antimicrobial peptide HPA3NT3-A2 to inhibit and reduce biofilm formation, eliminate EPS, and suppress inflammation in mice infected with clinical isolates of drug-resistant
Pseudomonas aeruginosa
strains. HPA3NT3-A2 was developed from a desirable analogue peptide, HPA3NT3, derived from residues 2-20 of the
Helicobacter pylori
ribosomal protein L1. HPA3NT3-A2 showed stronger activity against planktonic cells (MIC: 8 μM) compared to ciprofloxacin or tobramycin (>512 μM), and a favorable minimum biofilm inhibition and elimination concentration. This peptide also neutralized LPS; decreased levels of EPS; inhibited the production of pro-inflammatory cytokines in the lung, kidney, and spleen; decreased white blood cell counts; and increased survival among infected mice.
Bacterial biofilms formed through secretion of extracellular polymeric substances (EPS) have been implicated in many serious infections and can increase antibiotic resistance by a factor of more than 1000.</description><subject>Animals</subject><subject>Antibiotics</subject><subject>Antiinfectives and antibacterials</subject><subject>Antimicrobial Cationic Peptides - pharmacology</subject><subject>Biofilms</subject><subject>Biofilms - drug effects</subject><subject>Biofilms - growth & development</subject><subject>Cytokines</subject><subject>Drug resistance</subject><subject>Drug Resistance, Bacterial - drug effects</subject><subject>Extracellular Polymeric Substance Matrix - metabolism</subject><subject>Guinea Pigs</subject><subject>Leukocytes</subject><subject>Lipopolysaccharides - metabolism</subject><subject>Mice</subject><subject>Microbial Sensitivity Tests</subject><subject>Peptide Fragments - pharmacology</subject><subject>Peptides</subject><subject>Pseudomonas aeruginosa</subject><subject>Pseudomonas aeruginosa - cytology</subject><subject>Pseudomonas aeruginosa - drug effects</subject><subject>Pseudomonas aeruginosa - physiology</subject><subject>Resistance factors</subject><subject>Ribosomal Proteins - chemistry</subject><subject>Secretions</subject><subject>Spleen</subject><issn>2047-4830</issn><issn>2047-4849</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kUtPJCEUhYkZo0bduHfCZDbGpBTqUkWx7On4SnwtdF0BCkZMvQRK47-XtrVNXMjmEs6XE-45CO1RckQJiGMtVEcoKaheQ1s5YTxjFRO_Vncgm2g3hEeSDueClHQDbQItioJzvoWmWR9d57QflJMtHs0YXWPw-e0Mru8gm-XYWGt0dM-mfcWuf3DKxYCVG6xrO2wH38nohj5JONmYNBe4afCLiw-48dP_zJvgQpR9xEomyTu5g9atbIPZ_Zjb6P705G5-nl3enF3MZ5eZZoTFDADyUshSVJwBrygYosq0dNkoAKGYEIxUpSK60cqygjeK8vRWlaUFSaSFbXSw9B398DSZEOvOBW3aVvZmmEKd56KijDMKCf37DX0cJt-n39X5Ii4OQGmiDpdUCiwEb2w9etdJ_1pTUi_6qOfi39V7H_ME__6wnFRnmhX6mX4C_iwBH_RK_Sq0HpvFCvs_MfAGzMWZPA</recordid><startdate>20191119</startdate><enddate>20191119</enddate><creator>Lee, Jong-Kook</creator><creator>Mereuta, Loredana</creator><creator>Luchian, Tudor</creator><creator>Park, Yoonkyung</creator><general>Royal Society of Chemistry</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>7SR</scope><scope>8BQ</scope><scope>8FD</scope><scope>JG9</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-8717-3080</orcidid></search><sort><creationdate>20191119</creationdate><title>Antimicrobial peptide HPA3NT3-A2 effectively inhibits biofilm formation in mice infected with drug-resistant bacteria</title><author>Lee, Jong-Kook ; Mereuta, Loredana ; Luchian, Tudor ; Park, Yoonkyung</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c404t-333269a6987437813e0b60396db339b4994086b0cdcbf457db17994866f3a0af3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Animals</topic><topic>Antibiotics</topic><topic>Antiinfectives and antibacterials</topic><topic>Antimicrobial Cationic Peptides - pharmacology</topic><topic>Biofilms</topic><topic>Biofilms - drug effects</topic><topic>Biofilms - growth & development</topic><topic>Cytokines</topic><topic>Drug resistance</topic><topic>Drug Resistance, Bacterial - drug effects</topic><topic>Extracellular Polymeric Substance Matrix - metabolism</topic><topic>Guinea Pigs</topic><topic>Leukocytes</topic><topic>Lipopolysaccharides - metabolism</topic><topic>Mice</topic><topic>Microbial Sensitivity Tests</topic><topic>Peptide Fragments - pharmacology</topic><topic>Peptides</topic><topic>Pseudomonas aeruginosa</topic><topic>Pseudomonas aeruginosa - cytology</topic><topic>Pseudomonas aeruginosa - drug effects</topic><topic>Pseudomonas aeruginosa - physiology</topic><topic>Resistance factors</topic><topic>Ribosomal Proteins - chemistry</topic><topic>Secretions</topic><topic>Spleen</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lee, Jong-Kook</creatorcontrib><creatorcontrib>Mereuta, Loredana</creatorcontrib><creatorcontrib>Luchian, Tudor</creatorcontrib><creatorcontrib>Park, Yoonkyung</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Engineered Materials Abstracts</collection><collection>METADEX</collection><collection>Technology Research Database</collection><collection>Materials Research Database</collection><collection>MEDLINE - Academic</collection><jtitle>Biomaterials science</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lee, Jong-Kook</au><au>Mereuta, Loredana</au><au>Luchian, Tudor</au><au>Park, Yoonkyung</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Antimicrobial peptide HPA3NT3-A2 effectively inhibits biofilm formation in mice infected with drug-resistant bacteria</atitle><jtitle>Biomaterials science</jtitle><addtitle>Biomater Sci</addtitle><date>2019-11-19</date><risdate>2019</risdate><volume>7</volume><issue>12</issue><spage>568</spage><epage>583</epage><pages>568-583</pages><issn>2047-4830</issn><eissn>2047-4849</eissn><abstract>Bacterial biofilms formed through secretion of extracellular polymeric substances (EPS) have been implicated in many serious infections and can increase antibiotic resistance by a factor of more than 1000. Here, we examined the abilities of the antimicrobial peptide HPA3NT3-A2 to inhibit and reduce biofilm formation, eliminate EPS, and suppress inflammation in mice infected with clinical isolates of drug-resistant
Pseudomonas aeruginosa
strains. HPA3NT3-A2 was developed from a desirable analogue peptide, HPA3NT3, derived from residues 2-20 of the
Helicobacter pylori
ribosomal protein L1. HPA3NT3-A2 showed stronger activity against planktonic cells (MIC: 8 μM) compared to ciprofloxacin or tobramycin (>512 μM), and a favorable minimum biofilm inhibition and elimination concentration. This peptide also neutralized LPS; decreased levels of EPS; inhibited the production of pro-inflammatory cytokines in the lung, kidney, and spleen; decreased white blood cell counts; and increased survival among infected mice.
Bacterial biofilms formed through secretion of extracellular polymeric substances (EPS) have been implicated in many serious infections and can increase antibiotic resistance by a factor of more than 1000.</abstract><cop>England</cop><pub>Royal Society of Chemistry</pub><pmid>31555777</pmid><doi>10.1039/c9bm01051c</doi><tpages>16</tpages><orcidid>https://orcid.org/0000-0002-8717-3080</orcidid></addata></record> |
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| source | MEDLINE; Royal Society Of Chemistry Journals 2008- |
| subjects | Animals Antibiotics Antiinfectives and antibacterials Antimicrobial Cationic Peptides - pharmacology Biofilms Biofilms - drug effects Biofilms - growth & development Cytokines Drug resistance Drug Resistance, Bacterial - drug effects Extracellular Polymeric Substance Matrix - metabolism Guinea Pigs Leukocytes Lipopolysaccharides - metabolism Mice Microbial Sensitivity Tests Peptide Fragments - pharmacology Peptides Pseudomonas aeruginosa Pseudomonas aeruginosa - cytology Pseudomonas aeruginosa - drug effects Pseudomonas aeruginosa - physiology Resistance factors Ribosomal Proteins - chemistry Secretions Spleen |
| title | Antimicrobial peptide HPA3NT3-A2 effectively inhibits biofilm formation in mice infected with drug-resistant bacteria |
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