Asst Prof Chen Kaiwen


Asst Prof Chen Kaiwen
Assistant Professor
Department of Microbiology and Immunology
Tel: 6601 3848


Assistant Professor Chen Kaiwen obtained his PhD in Immunology in 2015 from the University of Queensland for his work on neutrophil inflammasomes. Subsequently, with the support a Marie Skłodowska-Curie Actions Incoming Postdoctoral Fellowship and a Swiss Government Excellence Fellowship (ESKAS), Kaiwen relocated to The University of Lausanne, Switzerland where he gained further expertise on cell death and inflammation. In 2020, Kaiwen is recruited to the Department of Microbiology and Immunology at NUS as an Assistant Professor.

What are your present research interests?

We are interested in understanding the complex cross talk between cell death and innate immune signalling, with the aim of rewiring cell death pathways to treat infectious diseases and inflammatory disorders.

What do you see as your future research directions?

A particular focus of the lab is gasdermins, a novel family of pore-forming proteins. We recently demonstrated that gasdermin D (GSDMD) promotes the extrusion of antimicrobial neutrophil extracellular traps (NETs) during cytosolic bacterial infection, but also mediates susceptibility to TNF-induced shock. We are now identifying novel regulators of these pathways using a combination of cell biology, biochemistry and animal models. We welcome enquiries from motivated Honours, PhD students and postdoctoral fellows!

Does your laboratory have a particularly strong research expertise?

Inflammasome, gasdermin, pyroptosis, NETosis, apoptosis, RIP kinase, TNF signalling and bacterial infection models.

Recent Publications

1. Caspase-8-dependent gasdermin D cleavage promotes anti-microbial defence but confers susceptibility to TNF-induced lethality. Demarco B, Grayczyk JP, Bjanes E, Le Roy D, Tonnus W, Assenmacher C-A, Radaelli E, Fettrelet T, Mack V, Linkermann A, Roger T, Brodsky IE, Chen KW#, Broz P#. Sci Adv, in press. #Corresponding authors
2. Pannexin-1 promotes NLRP3 activation during apoptosis but is dispensable for canonical or non‐canonical inflammasome activation. Chen KW#, Demarco B, Broz P#. Euro J Immunol, 2020, 50: 170–177. #Corresponding authors.
3. Extrinsic and intrinsic apoptosis activate Pannexin-1 to drive NLRP3 inflammasome assembly. Chen KW*, Demarco B*, Heilig R, Shkarina K, Boettcher A, Farady CJ, Pelczar P, Broz P. EMBO J, 2019, e101638. *equal contribution.
4. Noncanonical inflammasome signaling elicits gasdermin D–dependent neutrophil extracellular traps. Chen KW*, Monteleone M*, Boucher D*, Sollberger G, Ramnath D, Condon ND, von Pein JP, Broz P, Sweet MJ, Schroder K. Sci Immunol, 2018, 3, eaar6676. *equal contribution.
5. Cutting Edge: Blockade of Inhibitor of Apoptosis Proteins Sensitizes Neutrophils to TNF- but Not Lipopolysaccharide-Mediated Cell Death and IL-1beta Secretion. Chen KW, Lawlor KE, von Pein JB, Boucher D, Gerlic M, Croker BA, Bezbradica JS, Vince JE, and Schroder K. J Immunol, 2018, 200: 3341-3346.
6. Caspase-1 self-cleavage is an intrinsic mechanism to terminate inflammasome activity.
Boucher D, Monteleone M*, Coll RC*, Chen KW*, Ross CM, Teo JL, Gomez GA, Holley CL, Bierschenk D, Stacey KJ, Yap AS, Bezbradica JS, and Schroder K. J Exp Med, 2018, 215: 827-840. *equal contribution.
7. Active MLKL triggers the NLRP3 inflammasome in a cell-intrinsic manner. Conos SA, Chen KW, De Nardo D, Hara H, Whitehead L, Nunez G, Masters SL, Murphy JM, Schroder K, Vaux DL, Lawlor KE, Lindqvist LM, Vince JE. PNAS, 2017, 114: E961-E9.
8. The neutrophil NLRC4 inflammasome selectively promotes IL-1beta maturation without pyroptosis during acute Salmonella challenge. Chen KW, Gross CJ, Sotomayor FV, Stacey KJ, Tschopp J, Sweet MJ, Schroder K. Cell Reports, 2014, 8: 570-82.