Department of Immunology and Microbiology


Melody Neely
Associate Professor
(313) 577-1314

Melody N. Neely, Ph.D. is Associate Professor of Immunology and Microbiology. Previous to her arrival at Wayne State University School of Medicine, Dr. Neely did postdoctoral research at Washington University in St. Louis in the laboratory of Dr. Michael Caparon. She received her Ph.D. in Microbiology and Immunology from the University of Michigan in 1998.

The major research focus of Dr. Neely's laboratory involves elucidating mechanisms of microbial pathogenesis using several streptococcal pathogens as virulence models. During her postdoctoral research Dr. Neely developed a unique animal model system for the study of infectious disease using the zebrafish (Danio rerio) as a model host. In recent years the zebrafish has become a paradigm for the study of embryogenesis and vertebrate organ development as well as in studying human developmental diseases.

Streptococcal pathogens are the causative agents for a wide variety of different human diseases. Current research in the Neely lab utilizes the zebrafish model to study the virulence mechanisms involved in progression of different types of streptococcal infection. Streptococcus pyogenes is a human-specific pathogen reported to cause diseases ranging from the less serious impetigo and pharyngitis to the more serious invasive infections of cellulitis, necrotizing fasciitis and Streptococcal Toxic Shock Syndrome. Streptococcus iniae is a pathogen of fish as well as humans, causing cellulitis and necrotizing dermatitis as well as systemic infections leading to multiple organ failure and invasion into the cerebral spinal fluid. Both of these pathogens cause fatal infections in the zebrafish model, however they differ strikingly in the pathology of infection. S. pyogenes causes a localized necrotic infection while S. iniae causes a systemic infection with invasion into the blood stream and brain. This phenomenon allows us to address questions regarding the requirements for development and progression of different types of infectious disease. Identical types of infection showing very similar pathology occur in humans from various streptococcal pathogens resulting in serious morbidity and mortality. Some of the current research projects in the lab involve using multiple mutagenesis strategies to address specific virulence questions.

In addition, recent advances in the field of zebrafish genetics have highlighted the similarities of the zebrafish immune system to that of humans allowing us to address questions related to host response to infectious disease. The amenability of the zebrafish system to genetic manipulation allows us to directly address the host's role in progression of disease. Another interest in the laboratory is regulation of virulence gene expression. The regulatory mechanisms of several streptococcal virulence genes are currently being analyzed to determine how regulation plays a role in disease.

Research Interests
  • Zebrafish model of Streptococcal infections
  • Allen, J.P. and M. N. Neely. The Streptococcus iniae transcriptional regulator CpsY is required for protection from neutrophil-mediated killing and proper growth in vitro. Infect Immun. 80:1707-15. 2012 Medline
  • Hanson, B. R., B. A. Lowe, M.N. Neely. Membrane topology and DNA-binding ability of the Streptococcal CpsA protein. Journal of Bacteriology 193:411-420. 2011. Medline
  • Dmitriev A, Mohapatra SS, Chong P, Neely M, Biswas S, Biswas I. CovR-controlled global regulation of gene expression in Streptococcus mutans. PLoS One 6(5):e20127. 2011. Medline
  • Allen, J.P. and M.N. Neely. Trolling for the ideal model host: Zebrafish take the bait. Future Microbiology, 5(4):563-569. 2010. Medline
  • Kizy A. E. and M. N. Neely. First Streptococcus pyogenes Signature-Tagged Mutagenesis Screen Identifies Novel Virulence Determinants. Infection and Immunity 77:1854-1865. 2009. Medline
  • Kappeler K.V., S. Anbalagan, A.L. Dmitriev, E.J. McDowell, M.N. Neely and M. S. Chaussee. A naturally occurring Rgg variant in serotype M3 Streptococcus pyogenes does not activate speB expression due to altered specificity of DNA binding. Infection and Immunity 77:5411-5417. 2009. Medline
  • Phelps, H.A., D.R. Runft and M.N. Neely. Adult Zebrafish model of streptococcal infection. Current Protocols in Microbiology, Chapter 9: Unit 9D.1. 2009.
  • Locke, J.B., K.M. Colvin, A.K. Datta, S.K. Patel, N.N. Naidu, M.N. Neely, V. Nizet and J.T. Buchanan. Streptococcus iniae capsule impairs phagocytic clearance and contributes to virulence in fish. Journal of Bacteriology. 189:1279-1287. 2007. Medline
  • Lowe, B.A., J.D. Miller, and M.N. Neely. Analysis of the polysaccharide capsule of the systemic pathogen, Streptococcus iniae and its implications in virulence. Infection and Immunity. 75:1255-1264. 2007. Medline
  • Speshock, J.L., N. Doyon-Reale, R. Rabah, M.N. Neely and P.C. Roberts. Filamentous influenza A virus infection predisposes mice to fatal septicemia following superinfection with Streptococcus pneumoniae (serotype 3). Infection and Immunity. 75:3102-3111. 2007. Medline
  • Phelps, H.A., M.N. Neely. SalY of S. pyogenes lantibiotic locus is required for full virulence and intracellular survival in macrophages. Infection and Immunity. 75:4541- 4551. 2007. Medline


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