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John F. Bohnsack, MD Professor

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• Yale University - B.A. Molecular Biophysics and Biochemistry

• University of Virginia - M.D.

• University of Washington - Internship and Residency, Department of Pediatrics

• University of Washington Department of Pediatrics - Fellow, Division of Arthritis and Immunology

• National Institutes of Allergy and Infectious Diseases, NIH - Medical Staff Fellow, Laboratory of Clinical Investigation

• Scripps Clinic and Research Foundation - Research Associate, Department of Immunology

• American Board of Pediatrics

• American Board of Pediatrics, Pediatrics Rheumatology

• Attending Physician - University of Utah Medical Center

• Attending Physician - Primary Children's Medical Center

• Professor - University of Utah

• Thrasher Research Foundation Identivication of Pathogenic Group B Streptococci at Birth

• American Heart Association Grant-in-Aid Signal Pathways Involved in Neutrophil Alpha5Beta1 Interaction with Fibronectin

• USPHS Mechanisms of Host Resistance to Group B Streptococci

• USPHS Structure and Function of a Neutrophil Laminin Receptor

• Thrasher Research Foundation The Role of Secretory IgA in Protection Against Systemic Bacterial Infection

• Role of L-ficolin/mannose-binding lectin-associated serine protease complexes in the opsonophagocytosis of type III group B streptococci.
  Aoyagi, Y., E.E. Adderson, J.G. Min, M. Matsushita, T. Fujita, S. Takahashi, Y. Okuwaki, and J.F. Bohnsack.
  J Immunol, 2005. 174(1): p. 418-425.

• Fatal acute fibrinous and organizing pneumonia in a child with juvenile dermatomyositis.
  Prahalad, S., J.F. Bohnsack, C.G. Maloney, and K.O. Leslie.
  J Pediatr, 2005. 146(2): p. 289-292.

• Leukoencephalopathy, arthritis, colitis, and hypogammaglobulinemia (LACH) in two brothers: a novel syndrome?
  Bonkowsky, J.L., J.F. Bohnsack, M.J. Pennington, D. Viskochil, and J.A. Thompson.
  Am J Med Genet A, 2004. 128(1): p. 52-56.

• Familial aggregation of juvenile idiopathic arthritis.
  Prahalad, S., E. O'Brien, A.M. Fraser, R.A. Kerber, G.P. Mineau, D. Pratt, D. Donaldson, M.J. Bamshad, and J. Bohnsack.
  Arthritis Rheum, 2004. 50(12): p. 4022-4027.

• Equivalence of high-virulence clonotypes of serotype III group B Streptococcus agalactiae (GBS).
  Fleming, K.E., J.F. Bohnsack, G.C. Palacios, S. Takahashi, and E.E. Adderson.
  J Med Microbiol, 2004. 53(6): p. 505-508.

The Bohnsack laboratory studies host response and interactions with Group B streptococcus infections GBS), .a bacterial organism that infects human neonates and immunocompromised adults. Previous work characterized an enzyme produced by GBS that rapidly inactivates C5a, a potent complement derived pro-inflammatory mediator. Current work is directed at characterizing the population structure of GBS using molecular techniques, and establishing the relationship of the phylogenetic lineages to virulence. The ultimate goal is to understand the evolutionary origin of this pathogen and to devise novel strategies for preventing infections with the pathogen. Understanding the pathogenesis of neonatal GBS infections will also provide insights into the development of the neonatal immune system.