{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T05:05:27Z","timestamp":1791867927113,"version":"4.3.4"},"reference-count":47,"publisher":"American Society for Microbiology","issue":"6","license":[{"start":{"date-parts":[[2024,6,18]],"date-time":"2024-06-18T00:00:00Z","timestamp":1718668800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2024,6,18]],"date-time":"2024-06-18T00:00:00Z","timestamp":1718668800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"funder":[{"DOI":"10.13039\/501100001809","name":"MOST | National Natural Science Foundation of China","doi-asserted-by":"crossref","award":["32100135"],"award-info":[{"award-number":["32100135"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"crossref"}]},{"DOI":"10.13039\/501100001809","name":"MOST | National Natural Science Foundation of China","doi-asserted-by":"crossref","award":["32370190"],"award-info":[{"award-number":["32370190"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"crossref"}]},{"name":"MOST | National Key Research and Development Program of China","award":["2022YFC2303900"],"award-info":[{"award-number":["2022YFC2303900"]}]},{"name":"MOST | National Key Research and Development Program of China","award":["2022YFC3704700"],"award-info":[{"award-number":["2022YFC3704700"]}]}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["mSystems"],"published-print":{"date-parts":[[2024,6,18]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title\/>\n                    <jats:p>\n                      The emergence of nosocomial infections caused by hypervirulent and carbapenem-resistant\n                      <jats:italic>K. pneumoniae<\/jats:italic>\n                      (hv-CRKP) has become a significant public health challenge. The genetic traits of virulence and resistance plasmids in hv-CRKP have been extensively studied; however, research on the adaptive evolution strategies of clinical strains inside the host was scarce. This study aimed to understand the effects of antibiotic treatment on the phenotype and genotype characteristics of hv-CRKP. We investigated the evolution of hv-CRKP strains isolated from the same patient to elucidate the transition between hospital invasion and colonization. A comparative genomics analysis was performed to identify single nucleotide polymorphisms in the\n                      <jats:italic>rmpA<\/jats:italic>\n                      promoter. Subsequent validation through RNA-seq and gene deletion confirmed that distinct\n                      <jats:italic>rmpA<\/jats:italic>\n                      promoter sequences exert control over the mucoid phenotype. Additionally, biofilm experiments, cell adhesion assays, and animal infection models were conducted to illuminate the influence of\n                      <jats:italic>rmpA<\/jats:italic>\n                      promoter diversity on virulence changes. We demonstrated that the P12T and P11T promoters of\n                      <jats:italic>rmpA<\/jats:italic>\n                      possess strong activity, which leads to the evolution of CRKP into infectious and virulent strains. Meanwhile, the specific sequence of polyT motifs in the\n                      <jats:italic>rmpA<\/jats:italic>\n                      promoter led to a decrease in the lethality of hv-CRKP and enhanced cell adhesion and colonization. To summarize, the\n                      <jats:italic>rmpA<\/jats:italic>\n                      promoter of hv-CRKP is utilized to control capsule production, thereby modifying pathogenicity to better suit the host\u2019s ecological environment.\n                    <\/jats:p>\n                    <jats:sec>\n                      <jats:title>IMPORTANCE<\/jats:title>\n                      <jats:p>\n                        The prevalence of hospital-acquired illness caused by hypervirulent carbapenem-resistant\n                        <jats:italic>Klebsiella pneumoniae<\/jats:italic>\n                        (hv-CRKP) is significant, leading to prolonged antibiotic treatment. However, there are few reports on the phenotypic changes of hv-CRKP in patients undergoing antibiotic treatment. We performed a comprehensive examination of the genetic evolutionary traits of hv-CRKP obtained from the same patient and observed variations in the promoter sequences of the virulence factor\n                        <jats:italic>rmpA<\/jats:italic>\n                        . The strong activity of the promoter sequences P11T and P12T enhances the consistent production of capsule polysaccharides, resulting in an invasive strain. Conversely, weak promoter activity of P9T and P10T is advantageous for exposing pili, hence improving bacterial cell attachment ability and facilitating bacterial colonization. This finding also explains the confusion of some clinical strains carrying wild-type\n                        <jats:italic>rmpA<\/jats:italic>\n                        but exhibiting a low mucoid phenotype. This adaptive alteration facilitates the dissemination of\n                        <jats:italic>K. pneumoniae<\/jats:italic>\n                        within the hospital setting.\n                      <\/jats:p>\n                    <\/jats:sec>\n                  <\/jats:sec>","DOI":"10.1128\/msystems.01363-23","type":"journal-article","created":{"date-parts":[[2024,5,16]],"date-time":"2024-05-16T09:00:52Z","timestamp":1715850052000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":30,"title":["Adaptive attenuation of virulence in hypervirulent carbapenem-resistant\n                    <i>Klebsiella pneumoniae<\/i>"],"prefix":"10.1128","volume":"9","author":[{"given":"Gaoqin","family":"Teng","sequence":"first","affiliation":[{"name":"Department of Immunology and Pathogen Biology, School of Basic Medical Sciences, Hangzhou Normal University, Hangzhou, China"},{"name":"Key Laboratory of Multiple Organ Failure, Ministry of Education, Hangzhou, China"},{"name":"Department of General Intensive Care Unit of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Meng","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Immunology and Pathogen Biology, School of Basic Medical Sciences, Hangzhou Normal University, Hangzhou, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"YingYing","family":"Fu","sequence":"additional","affiliation":[{"name":"Department of Immunology and Pathogen Biology, School of Basic Medical Sciences, Hangzhou Normal University, Hangzhou, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaoqiang","family":"Yang","sequence":"additional","affiliation":[{"name":"Department of Immunology and Pathogen Biology, School of Basic Medical Sciences, Hangzhou Normal University, Hangzhou, 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