title: Implication of B lymphocytes in endotoxin-induced hepatic injury after partial hepatectomy in rats.
abstract: BACKGROUND
  Lymphocyte population constitutes major defense mechanism against endotoxemia, but the role of B lymphocytes in endotoxin-induced hepatic injury after hepatectomy is not clear.
  
  
  METHODS
  We used lymphopenic (L(-)) rats by single administration of anti-rat lymphocyte serum, nu/nu athymic (T(-)) rats, B cell-ablated (B(-))rats by intermittent injection of anti-immunoglobulin (Ig) micro-chain from birth, and their vehicle controls. These animals were subjected to two-thirds hepatectomy with subsequent intravenous lipopolysaccharides (LPS, 1.5 mg/kg) administration. The survival rate, plasma alanine transaminase (ALT), tumor necrosis factor-alpha (TNF-alpha) and IgM levels, and total hemolytic activity (CH50) were determined. Hepatic tissue deposition of IgM or C3 was assessed with immunohistochemistry.
  
  
  RESULTS
  The 24-h survival rate in control animals was 20%, whereas those in L(-), T(-), and B (-) animals were 80, 0, and 100%, respectively. Lymphocyte-sufficient control (L(+)) and B cell-sufficient control (B(+)) animals showed a rapid elevation of plasma TNF-alpha levels 1 h after the challenge, followed by an increase in plasma ALT levels. In B(+) group, plasma IgM levels were increased and CH50 activities were decreased 4 h after LPS injection with significant difference compared to those at time 0. Liver histology showed massive hepatic necrosis with a dense accumulation of IgM and C3 deposits 4 h after LPS administration. B cell ablation significantly ameliorated plasma ALT, IgM, and CH50 levels, showing less histological liver damage.
  
  
  CONCLUSIONS
  B lymphocytes susceptible to LPS might be implicated in the development of endotoxin-induced hepatic injury after partial hepatectomy.
authors.affiliation: Second Department of Surgery, Hamamatsu University School of Medicine, Handayama, Hamamatsu, Japan.
authors.forename: Atsuko
authors.initials: A
authors.lastname: Fukazawa
authors.forename: Yoshihiro
authors.initials: Y
authors.lastname: Yokoi
authors.forename: Kiyotaka
authors.initials: K
authors.lastname: Kurachi
authors.forename: Akihiro
authors.initials: A
authors.lastname: Uno
authors.forename: Shohachi
authors.initials: S
authors.lastname: Suzuki
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Konno
authors.forename: Satoshi
authors.initials: S
authors.lastname: Nakamura
mesh_terms: D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D000917:Antibody Formation / Q000502:physiology; D001402:B-Lymphocytes / Q000276:immunology*; D003176:Complement C3 / Q000378:metabolism; D019446:Endotoxemia / Q000276:immunology* / Q000401:mortality; D006498:Hepatectomy / Q000379:methods; D007075:Immunoglobulin M / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D008070:Lipopolysaccharides / Q000494:pharmacology; D008107:Liver Diseases / Q000276:immunology* / Q000401:mortality / Q000473:pathology; D008212:Lymphocyte Depletion; D008297:Male; D009336:Necrosis; D011183:Postoperative Complications / Q000276:immunology* / Q000401:mortality / Q000628:therapy; D051381:Rats; D011916:Rats, Inbred F344; D013047:Specific Pathogen-Free Organisms; D015996:Survival Rate; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D003176:Complement C3; D007075:Immunoglobulin M; D015850:Interleukin-6; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D000410:Alanine Transaminase