Bruce A. McClane, PhD
Professor
420 Bridgeside Point II
450 Technology Drive
Education
PhD in Microbiology, Pennsylvania State University
Research Summary
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.
Click here for a full listing of publications
Research Lab Affiliation
Publications
Shrestha A, Hendricks MR, Bomberger JM and McClane BA. 2016. Bystander Host Cell Killing Effects of Clostridium perfringens Enterotoxin. MBio. 7: pii: e02015-16. | View Abstract
Vidal JE, Ma M, Saputo J, Uzal FA and McClane BA. 2012. Evidence that the Agr-like quorum sensing system regulates the toxin production, cytotoxicity and pathogenicity of Clostridium perfringens type C isolate CN3685. Molec. Microbiol. 83: 179-194. | View Abstract
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. | View Abstract
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. Cell Microbiol. 11: 1306-1328. | View Abstract
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. | View Abstract