title: Lipopolysaccharide-induced bacterial translocation is intestine site-specific and associates with intestinal mucosal inflammation.
abstract: The present study aimed to determine whether any specific intestinal site or intestinal mucosal inflammation is highly correlated with bacterial translocation (BT). Enterostomy tubes were surgically placed in adult male Sprague-Dawley rats 5 days before induction of experimental model. After surgery, sterile water containing kanamycin (25 mg/L) was injected into each intestinal segment through the tubes for 3 days. Green fluorescent protein (GFP)-transfected Escherichia coli (n = 30 for lipopolysaccharide (LPS) group, and n = 30 for control group) or 0.9 % saline (n = 30 for blank group) were injected into each intestinal segment through the tubes for two consecutive days. Rats were then subjected to LPS-induced endotoxemia; lactulose and mannitol were injected into each intestinal segment through the tubes simultaneously. At 6 h after LPS injection, BT to distant organs and integrity of tight junctions (TJ) were examined by fluorescence and electron microscopy, respectively. The urinary excretion ratio of lactulose/mannitol (L/M) and intestinal mucosal cytokine levels were assessed. We found that the intestinal permeability, reflected by translocation rates of GFP-labeled E. coli, the levels of open TJ, the excretion ratio of L/M, and the inflammatory cytokine levels were higher in the LPS group than in the control and blank groups. The endotoxemia ileum showed the highest levels of both intestinal permeability and inflammatory cytokine, while the colon showed the lowest. The present study of endotoxemia rats suggests that LPS increases gut paracellular permeability and induces BT. The ileum is the site of greatest BT risk, while the colon is the lowest, and the difference in risk between these sites is correlated with intestinal mucosal inflammation.
authors: Research Institute of General Surgery, Jinling Hospital, Medical School of Nanjing University, 305 East Zhongshan Road, Nanjing, 210002, Jiangsu Province, China.
authors: Chao
authors: C
authors: Yue
authors: Bingqiang
authors: B
authors: Ma
authors: Yunzhao
authors: Y
authors: Zhao
authors: Qiurong
authors: Q
authors: Li
authors: Jieshou
authors: J
authors: Li
mesh_terms: D000818:Animals; D018988:Bacterial Translocation; D019446:Endotoxemia / Q000139:chemically induced; D004766:Enterostomy; D004926:Escherichia coli / Q000235:genetics / Q000472:pathogenicity; D004927:Escherichia coli Infections; D049452:Green Fluorescent Proteins; D007249:Inflammation / Q000382:microbiology*; D016753:Interleukin-10 / Q000378:metabolism; D015850:Interleukin-6 / Q000378:metabolism; D007413:Intestinal Mucosa / Q000276:immunology / Q000378:metabolism / Q000382:microbiology*; D007422:Intestines / Q000382:microbiology; D007612:Kanamycin / Q000494:pharmacology; D007792:Lactulose / Q000378:metabolism / Q000652:urine; D008070:Lipopolysaccharides; D008297:Male; D008353:Mannitol / Q000378:metabolism / Q000652:urine; D052016:Mucositis / Q000378:metabolism* / Q000382:microbiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D019108:Tight Junctions / Q000382:microbiology / Q000502:physiology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D015850:Interleukin-6; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D049452:Green Fluorescent Proteins; D008353:Mannitol; D007792:Lactulose; D007612:Kanamycin