title: Loss of hepatic B cells following lipopolysaccharide injection and polymicrobial sepsis.
abstract: OBJECTIVE
  B cells possess pleiotropic functions and are important for both humoral as well as cellular immune responses. However, there is little information about how hepatic B cells respond to lipopolysaccharide (LPS) and/or sepsis.
  
  
  METHODS
  We evaluated the changes in the number of hepatic and splenic B cells, and the expression of immunoglobulins after injecting pathogens, such as LPS, flagellin and CpG oligonucleotides in mice. In addition, we examined the role of natural killer (NK) cells in these changes using mutant bg/bg mice with genetically impaired NK cell functions.
  
  
  RESULTS
  Significant temporal loss of hepatic B cells, but not splenic B cells, was seen following LPS treatment. We have shown that bacterial components other than LPS were also responsible for such decline in hepatic B cells. However, loss of hepatic B cells was not seen following LPS treatment in bg/bg mice. In addition, loss of hepatic B cells and systemic immunoglobulin G2a production after LPS treatment was at least in part mediated by interleukin-12, gamma-interferon and tumor necrosis factor-alpha, all of which substantially enhanced the NK cell activity.
  
  
  CONCLUSIONS
  Hepatic B cells play an essential role during sepsis by synergistically interacting with NK cells. However, whether decline of hepatic B cells after LPS treatment and/or polymicrobial sepsis is simply a phenomenon or has a substantial clinical importance is yet to be determined.
authors.affiliation: Department of Immunology, The National Defence Medical College, Tokorozawa, Japan.
authors.forename: Atsushi
authors.initials: A
authors.lastname: Matsumoto
authors.forename: Hironori
authors.initials: H
authors.lastname: Tsujimoto
authors.forename: Satoshi
authors.initials: S
authors.lastname: Ono
authors.forename: Manabu
authors.initials: M
authors.lastname: Kinoshita
authors.forename: Yoshiko
authors.initials: Y
authors.lastname: Habu
authors.forename: Toshinobu
authors.initials: T
authors.lastname: Kawabata
authors.forename: Nariyoshi
authors.initials: N
authors.lastname: Shinomiya
authors.forename: Shuhji
authors.initials: S
authors.lastname: Seki
mesh_terms: D000818:Animals; D001402:B-Lymphocytes / Q000276:immunology*; D002432:Cecum / Q000601:surgery; D004195:Disease Models, Animal; D015536:Down-Regulation; D005408:Flagellin / Q000008:administration & dosage; D007074:Immunoglobulin G / Q000097:blood; D007274:Injections, Intraperitoneal; D007371:Interferon-gamma / Q000378:metabolism; D018664:Interleukin-12 / Q000378:metabolism; D007694:Killer Cells, Natural / Q000276:immunology; D008026:Ligation; D008070:Lipopolysaccharides / Q000008:administration & dosage; D008099:Liver / Q000276:immunology*; D008297:Male; D051379:Mice; D008809:Mice, Inbred C3H; D008810:Mice, Inbred C57BL; D008817:Mice, Mutant Strains; D009838:Oligodeoxyribonucleotides / Q000008:administration & dosage; D011677:Punctures; D018805:Sepsis / Q000209:etiology / Q000276:immunology*; D013154:Spleen / Q000276:immunology; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: C408982:CPG-oligonucleotide; D007074:Immunoglobulin G; D008070:Lipopolysaccharides; D009838:Oligodeoxyribonucleotides; D014409:Tumor Necrosis Factor-alpha; C440499:lipopolysaccharide, Escherichia coli O111 B4; D005408:Flagellin; D018664:Interleukin-12; D007371:Interferon-gamma