Chen Chen

BMB/CDIBChen Chen

M.D.:  Department of Clinical Medicine. Jining Medical College, China, 2001.
M.Sc.:  Department of Pathology, Shanghai Medical College, Fudan University, China, 2004.
Ph.D.: Department of Microbiology and Immunology, Medical College of Wisconsin, 2010.

Phone: 225-578-1555
Lab Phone: 225-578-5196
Office: A606 Life Sciences Annex
Lab: A621/A623/A625
E-mail: [email protected]    

Area of Interest:

Host-Pathogen interactions, Innate immunity, Bacterial toxins, Glycobiology.

The main goal of my laboratory is to understand how S. aureus seamlessly transitions between infection and colonization.   Although S. aureus colonization (30% of humans) is strongly associated with higher risks for clinical infections, most colonized individuals will not experience S. aureus infections, suggesting that S. aureus maintains a dedicated balance with the host.  

There are three areas of focus in the laboratory:

  1. To understand the molecular and cellular interactions between bacterial pathogens and hosts innate immune system, especially bacterial toxins and secreted proteins and their neutrophil manipulation activities.
  2. To understand the contribution of glycans for bacterial pathogenesis.
  3. To develop therapeutic and diagnostic platforms, using bacterial toxins and secreted proteins against human diseases.

I invite graduate and undergraduate students with an interest in my research to contact me.

Selected Publications:

Yang C, Dahms N, Barbieri JT, Chen C.  Multiple Domains of Staphylococcal Superantigen-like Protein 11 (SSL11) Contribute to Neutrophil Inhibition.  Biochemistry, 2022, 61(7): 616-624. 

Chen, C., Yang, C. & Barbieri, J. T. Staphylococcal Superantigen-like protein 11 mediates neutrophil adhesion and motility arrest, a unique bacterial toxin action. Sci Rep 9, 4211, doi:10.1038/s41598-019-40817-x (2019).

Chen C and Barbieri JT.  Detection of ADP-Ribosylating Bacterial Toxins (Book Chapter 20).  Methods Mol Biol. 1813:287-295, 2018.

Pellett S, Bradshaw M, Tepp WH, Pier CL, Whitemarsh RCM, Chen C, Barbieri JT, Johnson EA. The Light Chain Defines the Duration of Action of Botulinum Toxin Serotype A Subtypes.  mBio, 9(2), 00089-18, 2018

Chen C, Barbieri JT.  When Escherichia coli doesn’t fit the mold: A pertussis-like toxin with altered specificity.  J Biol Chem, 292(36), 15159-15160, 2017.

Chen C, Przedpelski A, Tepp WH, Pellett S, Johnson EA, Barbieri JT. Heat-Labile Enterotoxin IIa, a Platform To Deliver Heterologous Proteins into Neurons. mBio, 6, 00734-15, 2015.

Zuverink M, Chen C, Przedpelski A, Blum FC, Barbieri JT. A heterologous Reporter defines the Role of the Tetanus Toxin Interchain Disulfide in Light-Chain. Infect Immun.  83, 2714-24, 2015. 

Yang C, Chen C, Sorokin A. Prostaglandin E2 modifies SMAD2 and promotes SMAD2-SMAD4 complex formation. Prostaglandins Leukot Essent Fatty Acids. 90 145-9, 2014.

Chen C, Krishnan V, Macon K, Manne K, Narayana SV, Schneewind O. Secreted proteases control autolysin-mediated biofilm growth of Staphylococcus aureus. Journal of Biological Chemistry, 288 29440-52, 2013.

Blum FC, Chen C, Kroken AR, Barbieri JT. Tetanus toxin and botulinum toxin a utilize unique mechanisms to enter neurons of the central nervous system. Infect Immun. 80,1662-9, 2012.

Pier CL, Chen C, Tepp WH, Lin G, Janda KD, Barbieri JT, Pellett S, Johnson EA. Botulinum neurotoxin subtype A2 enters neuronal cells faster than subtype A1. FEBS Lett. 585,199-206, 2011.

Chen, C., Fu Z., Kim J.J., Barbieri, J. T. and Baldwin, M. R. Gangliosides as high affinity receptors for tetanus neurotoxin. Journal of Biological Chemistry, 284, 26569-577, 2009.

Fu Z., Chen C., Barbieri, J. T., Kim J.J., and Baldwin, M. R. Glycosylated SV2 and gangliosides as dual receptors for botulinum neurotoxin serotype F. Biochemistry, 48, 5631-41, 2009.

Chen C., Baldwin, M. R., and Barbieri, J. T. Molecular basis for tetanus toxin coreceptor interactions. Biochemistry, 47, 7179-86, 2008.

Chen C., Zhang J, Li J, Huang J, Yang C, Huang G, Shi J. Hydrodynamic-based in vivo transfection of retinoic X receptor- gene can enhance vitamin A-induced attenuation of liver fibrosis in mice. Liver International. 24: 679-686, 2004.