title: B Lymphocytes provide an infection niche for intracellular bacterium Brucella abortus.
abstract: BACKGROUND
  Brucella spp. are intracellular bacteria that establish lifelong infections whose mechanisms of chronicity are poorly understood. Notably, B cells facilitate the establishment of the high infection plateau that persists for months.
  
  
  METHODS
  We evaluated the contribution of murine B cells toward providing infection niches for Brucella by using flow cytometry and microscopy and by determining live bacterial counts associated with B cells both in vivo and in vitro.
  
  
  RESULTS
  Herein we demonstrate that immunoglobulin M and complement-opsonized Brucella abortus infects and survives inside primary murine B cells protected from bactericidal effects of gentamicin. The entry was dependent on microfilaments for internalization and subsequently brucellae reside in a late endosomal/lysosomal compartment. Throughout the infection, 10% of colony-forming units from infected mice was associated with B cells, and these cells transferred disease to naive hosts. Furthermore, Brucella-positive cells were positive for transforming growth factor (TGF) β1, and about 10% of such cells were B cells, similar to rates found for other intracellular pathogens that induce their hosts cells to produce TGF-β1.
  
  
  CONCLUSIONS
  To conclude, infected B cells contribute to chronic bacterial infections by providing an intracellular niche that may exert an immunoregulatory role. Although professional phagocytic cells harbor intracellular bacteria including Brucella, infection of lymphocytes by bacteria has not been previously appreciated.
authors.affiliation: Department of Veterinary and Animal Sciences, University of Massachusetts, Amherst, Massachusetts 01003, USA.
authors.forename: Radhika
authors.initials: R
authors.lastname: Goenka
authors.forename: Patrick D
authors.initials: PD
authors.lastname: Guirnalda
authors.forename: Samuel J
authors.initials: SJ
authors.lastname: Black
authors.forename: Cynthia L
authors.initials: CL
authors.lastname: Baldwin
mesh_terms: D000818:Animals; D000907:Antibodies, Bacterial / Q000276:immunology / Q000378:metabolism; D001402:B-Lymphocytes / Q000276:immunology* / Q000378:metabolism / Q000382:microbiology*; D002003:Brucella abortus / Q000235:genetics / Q000254:growth & development* / Q000276:immunology* / Q000378:metabolism; D002006:Brucellosis / Q000235:genetics / Q000276:immunology* / Q000378:metabolism / Q000382:microbiology*; D003165:Complement System Proteins / Q000276:immunology / Q000378:metabolism; D004261:DNA Replication / Q000235:genetics / Q000276:immunology; D011992:Endosomes / Q000235:genetics / Q000276:immunology / Q000378:metabolism / Q000382:microbiology; D007075:Immunoglobulin M / Q000276:immunology / Q000378:metabolism; D008247:Lysosomes / Q000235:genetics / Q000276:immunology / Q000378:metabolism / Q000382:microbiology; D008264:Macrophages / Q000276:immunology / Q000378:metabolism / Q000382:microbiology; D051379:Mice; D008807:Mice, Inbred BALB C; D009000:Monocytes / Q000276:immunology / Q000378:metabolism / Q000382:microbiology; D010587:Phagocytosis / Q000235:genetics / Q000276:immunology; D013234:Stem Cells / Q000276:immunology / Q000378:metabolism / Q000382:microbiology; D013534:Survival; D053773:Transforming Growth Factor beta1 / Q000276:immunology / Q000378:metabolism
chemical_list: D000907:Antibodies, Bacterial; D007075:Immunoglobulin M; D053773:Transforming Growth Factor beta1; D003165:Complement System Proteins