David L. Hasty, Ph.D.

David L. Hasty, Ph.D.

Department of Anatomy and Neurobiology


The University of Tennessee Health Science Center
1030 Jefferson Avenue
Memphis, TN 38104
Phone: (901) 523-8990, ext. 7556
Fax: (901) (901) 577-7273
Email: David L. Hasty


  • Ph.D. Institution: University of Tennessee Health Science Center, Memphis, TN
  • Postdoctoral: Harvard Medical School, Boston, MA

Research Interests

Research in my laboratory focuses on various aspects of the pathogenesis of infections caused by uropathogenic E. coli and group A streptococci. We have been interested for many years in the molecular mechanisms whereby these pathogenic bacteria attach to mucosal epithelial cells of the host. This involves identification of the adhesive surface proteins (adhesins) of the bacteria and their cognate receptors on the surfaces of host cells, as well as studying their molecular interactions. Molecular biological techniques have enabled us to clone adhesin genes, sequence allelic variants having different binding activities, inactivate the genes to create knockout strains and express fragments of the adhesin proteins to determine active motifs. Standard biochemical procedures have allowed us to purify adhesin and receptor proteins and to study the characteristics of their binding interactions. Experiments in animal models allow us to demonstrate the contribution of adhesins to pathogenesis of disease and to test anti-adhesion compounds to treat infections. Recently, we have begun to study the proinflammatory properties of various bacterial products and to determine the role this plays in activation of the innate immune system to either clear or exacerbate the infection. Current studies in this area deal with the synergistic interactions of streptococcal lipoteichoic acid and host blood components in the activation of macrophages to produce inflammatory cytokines.

Recent Publications

  • Penfound TA, Ofek I, Courtney HS, Hasty DL, Dale JB. The NH(2)-terminal region of Streptococcus pyogenes M5 protein confers protection against degradation by proteases and enhances mucosal colonization of mice. J Infect Dis. 2010 May 15;201(10):1580-8. PMID: 20367460
  • Cox KH, Ruiz-Bustos E, Courtney HS, Dale JB, Pence MA, Nizet V, Aziz RK, Gerling I, Price SM, Hasty DL. Inactivation of DltA modulates virulence factor expression in Streptococcus pyogenes. PLoS One. 2009;4(4):e5366. Epub 2009 Apr 29. PMID: 19401780
  • Courtney HS, Ofek I, Penfound T, Nizet V, Pence MA, Kreikemeyer B, Podbielski A, Hasty DL, Dale JB. Relationship between expression of the family of M proteins and lipoteichoic acid to hydrophobicity and biofilm formation in Streptococcus pyogenes. PLoS One. 2009;4(1):e4166. Epub 2009 Jan 9. Erratum in: PLoS ONE. 2009;28(2). doi: 10.1371/annotation/823215e6-c06a-4d5f-ac7b-0ee77067ccb2. PLoS ONE. 2009;4(1). doi: 10.1371/annotation/c2f3e4e5-b6a0-4be8-9f8c-3d4e01933385. Podbielbski, Andreas [corrected to Podbielski, Andreas]. PMID: 19132104
  • Meron-Sudai S, Matityahou A, Keisari Y, Cox KH, Hasty DL, Ofek I. Lipoteichoic acid synergizes with glycosphingolipids to potently stimulate secretion of interleukin-6 from human blood cells. Clin Vaccine Immunol. 2008 Sep;15(9):1309-15. Epub 2008 Jul 16. PMID: 18632923
  • Cox KH, Ofek I, Hasty DL. Enhancement of macrophage stimulation by lipoteichoic acid and the costimulant hemoglobin is dependent on Toll-like receptors 2 and 4. Infect Immun. 2007 May;75(5):2638-41. Epub 2007 Feb 12. PMID: 17296755
  • Hasty DL, Meron-Sudai S, Cox KH, Nagorna T, Ruiz-Bustos E, Losi E, Courtney HS, Mahrous EA, Lee R, Ofek I. Monocyte and macrophage activation by lipoteichoic Acid is independent of alanine and is potentiated by hemoglobin. J Immunol. 2006 May 1;176(9):5567-76. PMID: 16622026

View complete list of references (pubmed link)