Bruce A. McClane, PhD

  • Professor, Department of Microbiology and Molecular Genetics

Education & Training

  • Postdoc, NYU School of Medicine
  • PhD in Microbiology and Cell Biology, Penn State University

Research Interests

Our laboratory studies enteric diseases caused by Clostridium perfringens, including C. perfringens type A food poisoning, the 2nd most common bacterial foodborne illness, and antibiotic-associated diarrhea. Research projects underway in the lab include:
A. The mechanism of action of Clostridium perfringens enterotoxin. Clostridium perfringens enterotoxin (CPE) is responsible for the GI symptoms of C. perfringens type A enteric diseases. CPE binds to claudin receptors, oligomerizes into a hexamer on the plasma membrane surface of host cells, and then inserts into membranes to form an active pore. When cultures containing both CPE-sensitive and CPE-insensitive cells are treated with CPE, the sensitive cells release factors that kill the CPE-insensitive cells. This bystander killing effect is under study since it may contribute to pathogenesis by amplifying CPE activity in the body, where both CPE-sensitive and insensitive cells are present. RIP1 and RIP3 kinase involvement in CPE-induced cell death are also being examined. CPE is only produced during C. perfringens sporulation, so we are studying early steps in the sporulation pathway, a therapeutic target to prevent disease. We identified a key kinase that enhances sporulation and CPE production by >1000-fold. How this kinase affects sporulation is under study.
B. Pathogenic Contributions of Clostridium perfringens NanI Sialidase. NanI is the major sialidase of most C. perfringens strains. We are studying regulation of NanI sialidase production by C. perfringens and testing (with our collaborator at UC Davis) the importance of NanI for in vivo and in vitro growth and for intestinal growth, colonization and virulence.


Shrestha A, Hendricks MR, Bomberger JM and McClane BA. 2016. Bystander Host Cell Killing Effects of Clostridium perfringens Enterotoxin. MBio. 7: pii: e02015-16.

Vidal JE, Ma M, Saputo J, Uzal FA and McClane BA. 2012. Evidence that the agr quorum sensing system regulates the toxin production, cytotoxicity and pathogenicity of Clostridium perfringens type C isolate CN3685. Molec. Microbiol. 83: 179-194.

Li J, Sayeed S, Robertson S, Chen J and McClane BA. 2011. Sialidases affect the host cell adherence and epsilon toxin-induced cytotoxicity of Clostridium perfringens type D strain CN3718.  PLoS Pathogens. e1002429.

Vidal JE, Ohtani K, Shimizu T and McClane BA. 2009. Contact with enterocyte-like Caco-2 cells induces rapid upregulation of toxin production by Clostridium perfringens type C isolates. 2009. Cell. Microbiol. 11: 1306-1328.

Li J. and McClane BA. 2008. A novel small acid soluble protein variant is important for spore resistance of most Clostridium perfringens food poisoning isolates. PLoS Pathogens. 4: e1000056.

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