title: Gut bacterial translocation during total parenteral nutrition in experimental rats and its countermeasure.
abstract: BACKGROUND
  The use of total parenteral nutrition (TPN) is commonly associated with mucosal lining of the intestinal tract, causing degenerative changes within the gut-associated lymphoid tissue (GALT). These phenomena are probably caused by the translocation of indigenous intestinal bacteria into other organs and tissues where they induce infections.
  
  
  METHODS
  Using TPN model rats, this paper looks at the result of the investigation of the action of PSK (proteoglycan), a biological response modifier, which appears to suppress bacterial translocation and maintain local immunity activity.
  
  
  RESULTS
  Culture of mesenteric lymph nodes obtained post-TPN demonstrate a bacterial rate as high as 60%. Immunohistochemical examination indicates a reduction in the number of plasma cells and a decrease in S-IgA production and secretion. A similar reduction in S-IgA within bile and portal venous blood was also confirmed. Continuous oral administration of PSK in a daily dose of 1,000 mg/kg had a protective effect against the degeneration of GALT. A staining in immunocytes of Peyer's patches using immunohistochemical study was performed after administration of PSK and revealed constant levels of MHC-I, MHC-II, T helper cells, and interleukin-2 producing cells, supporting the protective role of PSK against degeneration of GALT with a subsequent reduction in bacterial translocation.
  
  
  CONCLUSIONS
  Proteoglycan can restore the impaired local immunity in the intestinal tract to normal levels and suppression of the bacterial translocation to provide an important function for patients receiving TPN treatment.
authors.affiliation: Department of Surgery, Tokai University Oiso Hospital, Kanagawa, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Nakasaki
authors.forename: T
authors.initials: T
authors.lastname: Mitomi
authors.forename: T
authors.initials: T
authors.lastname: Tajima
authors.forename: N
authors.initials: N
authors.lastname: Ohnishi
authors.forename: K
authors.initials: K
authors.lastname: Fujii
mesh_terms: D000284:Administration, Oral; D000818:Animals; D000911:Antibodies, Monoclonal; D001420:Bacteria, Aerobic / Q000302:isolation & purification; D001421:Bacteria, Anaerobic / Q000302:isolation & purification; D001431:Bacteriological Techniques; D001646:Bile / Q000276:immunology; D046508:Culture Techniques; D003627:Data Interpretation, Statistical; D004797:Enzyme-Linked Immunosorbent Assay; D006652:Histological Techniques; D007071:Immunoglobulin A, Secretory / Q000032:analysis / Q000097:blood; D007150:Immunohistochemistry; D007376:Interleukin-2 / Q000032:analysis; D007422:Intestines / Q000276:immunology / Q000382:microbiology*; D008099:Liver / Q000382:microbiology; D008198:Lymph Nodes / Q000276:immunology / Q000382:microbiology; D008221:Lymphoid Tissue / Q000187:drug effects / Q000276:immunology; D008285:Major Histocompatibility Complex; D008297:Male; D008643:Mesentery / Q000276:immunology / Q000382:microbiology; D010289:Parenteral Nutrition, Total / Q000009:adverse effects*; D010581:Peyer's Patches / Q000187:drug effects / Q000276:immunology; D011169:Portal Vein; D011509:Proteoglycans / Q000008:administration & dosage* / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D013154:Spleen / Q000382:microbiology; D013234:Stem Cells
chemical_list: D000911:Antibodies, Monoclonal; D007071:Immunoglobulin A, Secretory; D007376:Interleukin-2; D011509:Proteoglycans