title: Impact of Gastrointestinal Bacillus anthracis Infection on Hepatic B Cells.
abstract: Ingestion of Bacillus anthracis results in rapid gastrointestinal (GI) infection, known as GI anthrax. We previously showed that during GI anthrax, there is swift deterioration of intestinal barrier function leading to translocation of gut-associated bacteria into systemic circulation. Additionally, we described dysfunction in colonic B cells. In concordance with our previous studies, here, we report early migration of the Sterne strain of B. anthracis along with other gut-resident bacteria into the infected murine liver. Additionally, despite a global decrease in the B cell population, we observed an increase in both B-1a and marginal zone (MZ)-like B cells. Both of these cell types are capable of producing immunoglobulins against common pathogens and commensals, which act as a general antibody barrier before an antigen-specific antibody response. Accumulation of these cells in the liver was associated with an increase in chemokine expression. These data suggest that the presence of Sterne and other commensals in the liver trigger migration of MZ-like B cells from the spleen to the liver to neutralize systemic spread. Further research is required to evaluate the possible cause of their failure to clear the infection within the liver, including the potential role of dysfunctional mitogen-activated protein kinase (MAPK) signaling.
authors.affiliation: Department of Infectious Diseases and Pathology, College of Veterinary Medicine, University of Florida, Gainesville, FL 32608, USA. collioun@ufl.edu.|Division of Gastroenterology, Hepatology, and Nutrition, College of Medicine, University of Florida, Gainesville, FL 32608, USA. collioun@ufl.edu.
authors.forename: Natacha
authors.initials: N
authors.lastname: Colliou
authors.affiliation: Department of Infectious Diseases and Pathology, College of Veterinary Medicine, University of Florida, Gainesville, FL 32608, USA. sahayb@ufl.edu.|Division of Gastroenterology, Hepatology, and Nutrition, College of Medicine, University of Florida, Gainesville, FL 32608, USA. sahayb@ufl.edu.
authors.forename: Bikash
authors.initials: B
authors.lastname: Sahay
authors.affiliation: Department of Infectious Diseases and Pathology, College of Veterinary Medicine, University of Florida, Gainesville, FL 32608, USA. zadehm@ufl.edu.|Division of Gastroenterology, Hepatology, and Nutrition, College of Medicine, University of Florida, Gainesville, FL 32608, USA. zadehm@ufl.edu.
authors.forename: Mojgan
authors.initials: M
authors.lastname: Zadeh
authors.affiliation: Department of Physiological Sciences, College of Veterinary Medicine, University of Florida, Gainesville, FL 32610, USA. jlowen@ufl.edu.
authors.forename: Jennifer L
authors.initials: JL
authors.lastname: Owen
authors.affiliation: Department of Infectious Diseases and Pathology, College of Veterinary Medicine, University of Florida, Gainesville, FL 32608, USA. m.zadeh@ufl.edu.|Division of Gastroenterology, Hepatology, and Nutrition, College of Medicine, University of Florida, Gainesville, FL 32608, USA. m.zadeh@ufl.edu.
authors.forename: Mansour
authors.initials: M
authors.lastname: Mohamadzadeh
mesh_terms: D000818:Animals; D000881:Anthrax / Q000382:microbiology* / Q000473:pathology; D001402:B-Lymphocytes / Q000378:metabolism / Q000382:microbiology*; D001408:Bacillus anthracis / Q000378:metabolism*; D003106:Colon / Q000382:microbiology; D004195:Disease Models, Animal; D005767:Gastrointestinal Diseases / Q000382:microbiology* / Q000473:pathology; D041981:Gastrointestinal Tract / Q000382:microbiology* / Q000473:pathology; D008099:Liver / Q000382:microbiology; D051379:Mice; D013154:Spleen / Q000382:microbiology; D013171:Spores, Bacterial / Q000378:metabolism
keywords: B cells; gastrointestinal anthrax; innate lymphoid cells; liver