Clinical Microbiology: Open Access

Cell shape and peptidoglycan: The importance of fundamental processes in Campylobacter jejuni pathogenesis, disease etiology and new treatment strategies

Joint Event on 8^th Annual Congress on CLINICAL MICROBIOLOGY & INFECTIOUS DISEASES & 13^th World Congress on VIROLOGY, INFECTIONS AND OUTBREAKS

December 05-06, 2018 | Vancouver, Canada

Erin C Gaynor

The University of British Columbia, Canada

Keynote: Clin Microbiol

Abstract:

Campylobacter jejuni is a leading cause of bacterial diarrheal disease in the developed world and can cause more cases of gastroenteritis than Salmonella and E. coli yearly combined. Yet, its mechanisms of disease are still largely mysterious, as it lacks most hallmark virulence factors. Its characteristic corkscrew shape, however, had been historically thought to be important for its ability to burrow through the intestinal mucosa and asymptomatically colonize animal hosts such as birds and cause disease in susceptible hosts such as humans. But this had never been proven until recently. We performed a screen for C. jejuni mutants with alterations in cell surface polysaccharides. This led to the identification of the first C. jejuni gene shown to be required for its corkscrew shape. We named this gene pgp1, for ???peptidoglycan peptidase 1???, as Pgp1 was found to cleave peptidoglycan (PG) tripeptides to dipeptides. The Dpgp1 mutant is stick-straight and defective for chick colonization, motility and biofilm formation, while the Dpgp1 mutant PG hyper-stimulates Nod1, an innate immune system activator. Further studies showed that Dpgp1, as well as another stick-straight mutant, designated Dpgp2 (Pgp2 cleaves tetrapeptides to tripeptides), are defective for causing inflammation and penetrating deep into intestinal crypts in a mouse model of infection. A Pgp1 inhibitor has also been generated, which opens possibilities for new therapeutic avenues. Ongoing efforts to identify and characterize additional cell shape/PG-involved enzymes are providing exciting new research directions for our and related groups??? efforts to tackle this and other enigmatic pathogens.

Biography :

Erin Gaynor completed her PhD at the University of California, San Diego, working on yeast protein trafficking in the lab of Dr Scott Emr. She switched fields to microbiology and infectious diseases for her postdoctoral studies, which were performed at Stanford University under the supervision of Dr Stanley Falkow. She is currently a Professor in Microbiology & Immunology at the University of British Columbia and has published more than 50 papers in high-ranking journals. She sits on grant committee panels, enjoys teaching both in the lab and classroom and has been an editor and/or reviewer for numerous journals.

E-mail: egaynor@mail.ubc.ca