{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,9]],"date-time":"2026-09-09T12:34:35Z","timestamp":1788957275553,"version":"build-2803163510"},"reference-count":26,"publisher":"American Society for Microbiology","issue":"5","license":[{"start":{"date-parts":[[2014,5,1]],"date-time":"2014-05-01T00:00:00Z","timestamp":1398902400000},"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":["Infect Immun"],"published-print":{"date-parts":[[2014,5]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            Prior antibiotic exposure is associated with increased mortality in Gram-negative bacteria-induced sepsis. However, how antibiotic-mediated changes of commensal bacteria promote the spread of enteric pathogenic bacteria in patients remains unclear. In this study, the effects of systemic antibiotic treatment with or without Toll-like receptor (TLR) stimulation on bacterium-killing activity, antibacterial protein expression in the intestinal mucosa, and bacterial translocation were examined in mice receiving antibiotics with or without oral supplementation of dead\n            <jats:named-content content-type=\"genus-species\">Escherichia coli<\/jats:named-content>\n            or\n            <jats:named-content content-type=\"genus-species\">Staphylococcus aureus<\/jats:named-content>\n            . We developed a systemic ampicillin, vancomycin, and metronidazole treatment protocol to simulate the clinical use of antibiotics. Antibiotic treatment decreased the total number of bacteria, including aerobic bacteria belonging to the family\n            <jats:named-content content-type=\"genus-species\">Enterobacteriaceae<\/jats:named-content>\n            and the genus\n            <jats:named-content content-type=\"genus-species\">Enterococcus<\/jats:named-content>\n            as well as organisms of the anaerobic genera\n            <jats:named-content content-type=\"genus-species\">Lactococcus<\/jats:named-content>\n            and\n            <jats:named-content content-type=\"genus-species\">Bifidobacterium<\/jats:named-content>\n            in the intestinal mucosa and lumen. Antibiotic treatment significantly decreased the bacterium-killing activity of the intestinal mucosa and the expression of non-defensin-family proteins, such as RegIII\u03b2, RegIII\u03b3, C-reactive protein-ductin, and RELM\u03b2, but not the defensin-family proteins, and increased\n            <jats:named-content content-type=\"genus-species\">Klebsiella pneumoniae<\/jats:named-content>\n            translocation. TLR stimulation after antibiotic treatment increased NF-\u03baB DNA binding activity, nondefensin protein expression, and bacterium-killing activity in the intestinal mucosa and decreased\n            <jats:named-content content-type=\"genus-species\">K. pneumoniae<\/jats:named-content>\n            translocation. Moreover, germfree mice showed a significant decrease in nondefensin proteins as well as intestinal defense against pathogen translocation. Since TLR stimulation induced NF-\u03baB DNA binding activity, TLR4 expression, and mucosal bacterium-killing activity in germfree mice, we conclude that the commensal microflora is critical in maintaining intestinal nondefensin protein expression and the intestinal barrier. In turn, we suggest that TLR stimulation induces nondefensin protein expression and reverses antibiotic-induced gut defense impairment.\n          <\/jats:p>","DOI":"10.1128\/iai.01578-14","type":"journal-article","created":{"date-parts":[[2014,3,5]],"date-time":"2014-03-05T04:44:48Z","timestamp":1393994688000},"page":"1994-2005","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":30,"title":["Toll-Like Receptor Stimulation Induces Nondefensin Protein Expression and Reverses Antibiotic-Induced Gut Defense Impairment"],"prefix":"10.1128","volume":"82","author":[{"given":"Ying-Ying","family":"Wu","sequence":"first","affiliation":[{"name":"Department of Biological Sciences, National Sun Yat-Sen University, Kaohsiung, Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ching-Mei","family":"Hsu","sequence":"additional","affiliation":[{"name":"Department of Biological Sciences, National Sun Yat-Sen University, Kaohsiung, Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pei-Hsuan","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Surgery, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chang-Phone","family":"Fung","sequence":"additional","affiliation":[{"name":"Division of Infectious Diseases, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan"},{"name":"Institute of Emergency and Critical Care Medicine, National Yang-Ming University, Taipei, Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lee-Wei","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Surgery, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan"},{"name":"Institute of Emergency and Critical Care Medicine, National Yang-Ming University, Taipei, Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.01520-08"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1038\/nrmicro1978"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1097\/SHK.0b013e31816a3458"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.ijmm.2007.03.010"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1038\/nri2316"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.immuni.2010.02.012"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1136\/gut.2007.141481"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.1038\/nature07250"},{"key":"e_1_3_2_10_2","doi-asserted-by":"publisher","DOI":"10.1007\/s10096-010-0931-1"},{"key":"e_1_3_2_11_2","doi-asserted-by":"publisher","DOI":"10.1097\/CCM.0b013e31821b85f4"},{"key":"e_1_3_2_12_2","first-page":"51","article-title":"An experimental model for studying reversible intestinal ischemia","volume":"153","author":"Otamiri T","year":"1987","unstructured":"OtamiriTSjodahlRTagessonC. 1987. 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Transferable antibiotic resistance in E. coli and Klebsiella pneumoniae. Can. Med. Assoc. J. 109:691\u2013696.","journal-title":"Can. Med. Assoc. 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