title: Dead bacteria reverse antibiotic-induced host defense impairment in burns.
abstract: BACKGROUND
  Burn patients can incur high rates of hospital-acquired infections. The mechanism of antibiotic exposure on inducing infection vulnerability has not been determined. This study aimed to examine the effects of antibiotic treatment on host defense mechanisms.
  
  
  METHODS
  First we treated C57/BL6 mice with combined antibiotic treatment after 30% to 35% total body surface area burn. Animals were sacrificed at 48 hours after sham or thermal injury treatment. Bacterial counts in intestinal lumen and mucosa were measured. Next, we treated animals with or without oral dead Escherichia coli or Staphylococcus aureus supplementation to stimulate Toll-like receptor in the intestinal mucosa. Toll-like receptor 4, antibacterial protein expression, nuclear factor (NF)-κB DNA-binding activity, and bacteria-killing activity in the intestinal mucosa; intestinal permeability; bacterial translocation to mesenteric lymph nodes; Klebsiella pneumoniae translocation; interleukin-6 in the blood; and phagocytic activity of alveolar macrophages, were assessed.
  
  
  RESULTS
  Thermal injury increased microflora and NF-κB DNA-binding activity of the intestine. Systemic antibiotic treatment decreased gut microflora and increased bacterial translocation to mesenteric lymph nodes, intestinal permeability, and interleukin-6 levels in the blood. Antibiotic treatment also decreased bacteria-killing activity in intestinal mucosa and phagocytic activity of alveolar macrophages. Oral dead E coli and S aureus supplementation induced NF-κB DNA-binding activity, Toll-like receptor 4, and antibacterial protein expression of the intestinal mucosa.
  
  
  CONCLUSIONS
  Taken together with the fact that dead bacteria reversed antibiotic-induced K pneumoniae translocation and intestinal and pulmonary defense impairment, we conclude that combined antibiotic treatment results in systemic host defense impairment in burns through the decrease in intestinal flora. We suggest that dead bacteria supplementation could induce nondefensin protein expression and reverse antibiotic-induced gut and lung defense impairment in burn patients.
authors.affiliation: Department of Surgery, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan; Institute of Emergency and Critical Care Medicine, National Yang-Ming University, Taipei, Taiwan.
authors.forename: Lee-Wei
authors.initials: LW
authors.lastname: Chen
authors.affiliation: Department of Surgery, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan.
authors.forename: Pei-Hsuan
authors.initials: PH
authors.lastname: Chen
authors.affiliation: Institute of Emergency and Critical Care Medicine, National Yang-Ming University, Taipei, Taiwan; Division of Infectious Diseases, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan.
authors.forename: Chang-Phone
authors.initials: CP
authors.lastname: Fung
authors.affiliation: Department of Biological Sciences, National Sun Yat-Sen University, Kaohsiung, Taiwan. Electronic address: chingmei@mail.nsysu.edu.tw.
authors.forename: Ching-Mei
authors.initials: CM
authors.lastname: Hsu
mesh_terms: D000818:Animals; D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D001419:Bacteria / Q000276:immunology*; D018988:Bacterial Translocation / Q000187:drug effects; D015153:Blotting, Western; D002056:Burns / Q000276:immunology / Q000378:metabolism / Q000382:microbiology; D004195:Disease Models, Animal; D004797:Enzyme-Linked Immunosorbent Assay; D007082:Ileum / Q000187:drug effects / Q000378:metabolism / Q000382:microbiology; D007113:Immunity, Innate; D007413:Intestinal Mucosa / Q000276:immunology / Q000378:metabolism / Q000382:microbiology*; D008198:Lymph Nodes / Q000382:microbiology; D008297:Male; D008643:Mesentery; D051379:Mice; D008810:Mice, Inbred C57BL; D016328:NF-kappa B / Q000378:metabolism; D010587:Phagocytosis; D051197:Toll-Like Receptor 4 / Q000096:biosynthesis / Q000276:immunology*; D014946:Wound Infection / Q000276:immunology* / Q000382:microbiology / Q000517:prevention & control
chemical_list: D000900:Anti-Bacterial Agents; D016328:NF-kappa B; D051197:Toll-Like Receptor 4