{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,30]],"date-time":"2026-07-30T09:59:57Z","timestamp":1785405597833,"version":"3.56.0"},"reference-count":56,"publisher":"American Society for Microbiology","issue":"11","license":[{"start":{"date-parts":[[2025,11,4]],"date-time":"2025-11-04T00:00:00Z","timestamp":1762214400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2025,11,4]],"date-time":"2025-11-04T00:00:00Z","timestamp":1762214400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Microbiol Spectr"],"published-print":{"date-parts":[[2025,11,4]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title\/>\n                    <jats:p>\n                      Polydextrose (PDX), as a prebiotic, is an extensively branched glucose polymer that can promote the growth of beneficial bacteria in the gut. Recent research indicates that PDX regulates intestinal function and supports immune balance, which helps to protect the gut from pathogenic bacteria. However, scarce research has been found that PDX prevents the host infection through the direct effects on the pathogen. In this study, we developed a mouse model infected with\n                      <jats:italic toggle=\"yes\">Klebsiella pneumoniae<\/jats:italic>\n                      by pretreating with PDX, assessed the effect of PDX on\n                      <jats:italic toggle=\"yes\">K. pneumoniae<\/jats:italic>\n                      acute infection in mice, and explored its potential mechanisms. We developed a mouse model that is infected with\n                      <jats:italic toggle=\"yes\">K. pneumoniae<\/jats:italic>\n                      by pretreating with PDX. Colony counting quantified the\n                      <jats:italic toggle=\"yes\">K. pneumoniae<\/jats:italic>\n                      bacterial load in the parenchymal organs of mice. A scanning electron microscope was used to investigate the morphological characteristics of\n                      <jats:italic toggle=\"yes\">K. pneumoniae<\/jats:italic>\n                      . The expression level of TamA (translocation and assembly module A) was detected by reverse transcription-polymerase chain reaction (RT-PCR) and western blotting. The CRISPR-Cas9 technique was applied to construct the\n                      <jats:italic toggle=\"yes\">tamA<\/jats:italic>\n                      mutant strains (\u0394\n                      <jats:italic toggle=\"yes\">tamA<\/jats:italic>\n                      ) and the\n                      <jats:italic toggle=\"yes\">tamA<\/jats:italic>\n                      complement strain (\n                      <jats:italic toggle=\"yes\">C-<\/jats:italic>\n                      \u0394\n                      <jats:italic toggle=\"yes\">tamA<\/jats:italic>\n                      ). The biofilm formation capacity was evaluated by the crystal violet assay. The capsule production was quantified by measuring uronic acid content. In the PDX pretreated model, PDX did not alter the growth characteristics and morphological structure of\n                      <jats:italic toggle=\"yes\">K. pneumoniae<\/jats:italic>\n                      . However, it significantly reduces the load of\n                      <jats:italic toggle=\"yes\">K. pneumoniae<\/jats:italic>\n                      in the lung, liver, spleen, and intestinal tract of mice, which is related to inhibiting the expression of the outer membrane TamA protein by PDX. In an\n                      <jats:italic toggle=\"yes\">in vitro<\/jats:italic>\n                      study, the results indicated that deletion of\n                      <jats:italic toggle=\"yes\">tamA<\/jats:italic>\n                      significantly inhibited capsule production and biofilm formation of\n                      <jats:italic toggle=\"yes\">K. pneumoniae<\/jats:italic>\n                      , weakened interspecific and intraspecific competitive abilities with other members of the\n                      <jats:italic toggle=\"yes\">Enterobacteriaceae<\/jats:italic>\n                      family, and reduced the adhesion ability to Caco-2 and murine lung epithelial (MLE) cells. Compared with the wild strain, PDX treatment and the deletion of\n                      <jats:italic toggle=\"yes\">tamA<\/jats:italic>\n                      inhibit the expression of adhesion factors (including\n                      <jats:italic toggle=\"yes\">FimH<\/jats:italic>\n                      ,\n                      <jats:italic toggle=\"yes\">FimC<\/jats:italic>\n                      ,\n                      <jats:italic toggle=\"yes\">FimD<\/jats:italic>\n                      , and\n                      <jats:italic toggle=\"yes\">MrkD<\/jats:italic>\n                      ) and the capsule synthesis genes (including\n                      <jats:italic toggle=\"yes\">galF<\/jats:italic>\n                      ,\n                      <jats:italic toggle=\"yes\">wzi<\/jats:italic>\n                      , and\n                      <jats:italic toggle=\"yes\">manC<\/jats:italic>\n                      ) in\n                      <jats:italic toggle=\"yes\">K. pneumoniae<\/jats:italic>\n                      . PDX can prevent the infection of\n                      <jats:italic toggle=\"yes\">K. pneumoniae<\/jats:italic>\n                      in mice. The potential mechanism may involve downregulating TamA expression and inhibiting adhesion-related molecules. Therefore, PDX can serve as a potential prebiotic to reduce\n                      <jats:italic toggle=\"yes\">K. pneumoniae<\/jats:italic>\n                      infections in both humans and animals.\n                    <\/jats:p>\n                    <jats:sec>\n                      <jats:title>IMPORTANCE<\/jats:title>\n                      <jats:p>\n                        Our findings revealed that polydextrose (PDX) could significantly reduce the load of\n                        <jats:italic toggle=\"yes\">Klebsiella pneumoniae<\/jats:italic>\n                        in the lung, liver, spleen, and intestinal tract of mice. The potential mechanism is related to inhibiting the expression of the outer membrane TamA protein by PDX. The deletion of\n                        <jats:italic toggle=\"yes\">tamA<\/jats:italic>\n                        significantly inhibited the capsule production and biofilm formation of\n                        <jats:italic toggle=\"yes\">K. pneumoniae<\/jats:italic>\n                        , weakened the interspecific and intraspecific competitiveness ability with other members of the\n                        <jats:italic toggle=\"yes\">Enterobacteriaceae<\/jats:italic>\n                        family, and reduced the adhesion ability to Caco-2 and MLE cells. Our data suggest that PDX may act as a prebiotic to reduce\n                        <jats:italic toggle=\"yes\">K. pneumoniae<\/jats:italic>\n                        infections in humans and animals.\n                      <\/jats:p>\n                    <\/jats:sec>\n                  <\/jats:sec>","DOI":"10.1128\/spectrum.01017-25","type":"journal-article","created":{"date-parts":[[2025,10,1]],"date-time":"2025-10-01T13:01:21Z","timestamp":1759323681000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":3,"title":["Polydextrose reduces the infection of\n                    <i>Klebsiella pneumoniae<\/i>\n                    in mice by downregulating the expression of TamA"],"prefix":"10.1128","volume":"13","author":[{"given":"Lin","family":"Su","sequence":"first","affiliation":[{"name":"Henan Collaborative Innovation Center of Prevention and Treatment of Mental Disorders, Henan Key Laboratory of Biological Psychiatry, 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