title: Inflammatory consequences of the translocation of bacteria and endotoxin to mesenteric lymph nodes.
abstract: BACKGROUND
  Translocation of intestinal bacteria to mesenteric lymph nodes (MLNs) has been documented in humans under a variety of circumstances, yet its clinical significance remains to be established. The aim of this study was to correlate detectable translocation to MLNs of bacteria and endotoxin with local and systemic signs of inflammation.
  
  
  METHODS
  From each of 10 patients with carcinoma of the cecal region two MLNs were harvested prior to resection. The presence of bacteria and endotoxin in the lymphatic tissue and blood was determined by culture methods and DNA preparation (PCR) and by a Limulus assay, respectively. Inflammatory mediators were determined in plasma and in MLN homogenates.
  
  
  RESULTS
  Viable bacteria were detected in MLNs of 7 patients and in 9 of 20 lymph nodes. PCR revealed traces of bacteria in 4 patients and in 6 of their MLNs. Combining both modalities, the translocation rate was 80% and 55% for patients and MLNs, respectively. There was no detectable bacteremia. Endotoxin was found in the plasma of 7 patients and in 9 MLNs from 5 patients. There was no correlation between culture findings and endotoxin concentrations. Moreover, bacteriological data did not correspond to local or systemic inflammation. The group of MLN with detectable endotoxin differed significantly from LPS-negative nodes with respect to interleukin-6, interleukin-10, and sCD14. Systemic concentrations of endotoxin and inflammatory parameters did not correspond to levels within MLNs.
  
  
  CONCLUSIONS
  Translocation to MLNs occurs in patients with cecal carcinoma. This, however, seems not to be of major clinical significance if no additional physiologic insults are encountered. Irrespective of the presence of bacteria, there are variations in inflammatory reactions between lymph nodes from one and the same patient, probably reflecting fluctuating response mechanisms to low-grade translocation.
authors.affiliation: Department of Surgery, University of Freiburg, Freiburg, Germany.
authors.forename: U
authors.initials: U
authors.lastname: Schoeffel
authors.forename: K
authors.initials: K
authors.lastname: Pelz
authors.forename: R U
authors.initials: RU
authors.lastname: Häring
authors.forename: R
authors.initials: R
authors.lastname: Amberg
authors.forename: R
authors.initials: R
authors.lastname: Schandl
authors.forename: R
authors.initials: R
authors.lastname: Urbaschek
authors.forename: B U
authors.initials: BU
authors.lastname: von Specht
authors.forename: E H
authors.initials: EH
authors.lastname: Farthmann
mesh_terms: D000704:Analysis of Variance; D016470:Bacteremia / Q000382:microbiology; D018988:Bacterial Translocation / Q000502:physiology*; D001431:Bacteriological Techniques; D002277:Carcinoma / Q000382:microbiology; D002430:Cecal Neoplasms / Q000382:microbiology; D003110:Colonic Neoplasms / Q000382:microbiology; D004731:Endotoxins / Q000032:analysis* / Q000097:blood; D006801:Humans; D018836:Inflammation Mediators / Q000032:analysis / Q000097:blood; D016753:Interleukin-10 / Q000032:analysis; D015850:Interleukin-6 / Q000032:analysis; D018950:Lipopolysaccharide Receptors / Q000032:analysis; D008070:Lipopolysaccharides / Q000032:analysis; D008198:Lymph Nodes / Q000378:metabolism / Q000382:microbiology*; D008640:Mesenteric Lymphadenitis / Q000378:metabolism / Q000382:microbiology*; D008643:Mesentery; D016133:Polymerase Chain Reaction; D018709:Statistics, Nonparametric
chemical_list: D004731:Endotoxins; D018836:Inflammation Mediators; D015850:Interleukin-6; D018950:Lipopolysaccharide Receptors; D008070:Lipopolysaccharides; D016753:Interleukin-10