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About Sickkids
About SickKids

Nicola Jones, MD, PhD, FRCP(C)

The Hospital for Sick Children
Staff Gastroenterologist
Gastroenterology, Hepatology and Nutrition

Research Institute
Senior Scientist
Cell Biology

University of Toronto
Department of Paediatrics and Physiology

Phone: 416-813-7733
Fax: 416-813-6531
Alternate Contact: Thusiga Inderanathan
Alternate Email: thusiga.inderanathan@sickkids.ca

For more information, visit:

Jones Lab website

Brief Biography

Dr. Nicola Jones is a Senior Scientist in the Cell Biology Program and a Staff Gastroenterologist in the Division of Gstroneterology, Hepatology and Nutrition at Sickkids.  Dr. Nicola Jones completed medical school at the University of Toronto in 1989 and training in paediatrics at The Hospital for Sick Children in Toronto in 1993. She completed clinical subspecialty training in gastroenterology at The Hospital for Sick Children (1993-1994) and subsequently underwent research training with completion of a PhD in Molecular and Medical Genetics at the University of Toronto (1995-1999). Dr. Jones research program focuses on host pathogen interactions and understanding mechanisms of infection and inflammatory mediated disease including Inflammatory Bowel disease and cancer.

Dr. Jones also has a strong interest in the education and career development of clinician scientists and is the Principal Investigator for the Canadian Child Health Clinician Scientist Program, an interdisciplinary training program aimed and developing the next generation of clinician scientists in child and youth health across Canada.

Research Interests

  • Helicobacter pylori infection
  • Inflammatory bowel disease
  • Infection and inflammation-mediated cancer

Research Activities

The central theme of Dr. Jones research focuses on understanding cellular and molecular mechanisms involved in infection- and inflammation- mediated gastroenteric diseases including Helicobacter pylori infection, inflammatory bowel disease and inflammation-mediated cancers.

Helicobacter pylori infection: Half of the world’s human population is infected with H. pylori. Chronic H. pylori infection is the most significant risk factor for the development of gastric cancer, one of the leading causes of cancer-related deaths worldwide. My laboratory investigates the mechanisms by which H. pylori evades the host immune system to promote chronic infection as well as the underlying mechanisms by which bacterial virulence factors manipulate host responses to cause gastric cancer.

Inflammatory Bowel Disease: Canada has amongst the highest rates of inflammatory bowel disease in the world. Importantly over the past two decades these rates are increasing especially in the young. These findings suggest that environmental factors may be involved in this increase. My laboratory is studying underlying mechanisms promoting inflammatory bowel disease with a particular interest in the autophagy pathway. In addition we are delineating the cellular and molecular mechanisms by which the environment might modulate risk for disease.

Inflammation –mediated cancers: Inflammation is a known risk factor for the development of cancer. My laboratory investigates underlying cellular and molecular mechanisms by which microbes and inflammation promote development of gastric and colorectal cancers.

External Funding

  • CIHR Canadian Child Health Clinician Scientist Training Program. Jones NL: Strategic Training Initiative in Health Research, Canadian Institutes of Health Research. 2012-2015
  • Canadian Pediatric Clinician Scientist Program. Jones NL: The Hospital for Sick Children Foundation. 2012-2015
  • Canadian Pediatric Clinician Scientist Program. Jones NL: BC Research Institute for Children and Women’s Health. 2012-2015
  • Canadian Pediatric Clinician Scientist Program. Jones NL: Women’s and Children’s Health Research Institute. 2012-2015
  • Canadian Pediatric Clinician Scientist Program. Jones NL: Manitoba Institute of Child Health. 2012-2015
  • Role of ATG16L1 in Crohn disease. Jones NL: Crohn’s and Colitis Foundation of Canada. 2012-2014
  • Role of autophagy during H. pylori infection and disease. Jones NL: Canadian Institutes of Health Research. 2008-2013


  • Canadian Association of Gastroenterology Education Excellence Award 2014
  • Canadian Association of Gastroenterology Visiting Research Scientist Award 2013
  • Canadian Association of Gastroenterology Young Educator Award 2009
  • Canadian Association of Gastroenterology Young Investigator Award 2005


For a complete list of publications see PubMed.

Helicobacter pylori inhibits dendritic cell maturation via interleukin-10 mediated activation of the signal transducer and activator of transcription 3 (STAT3) pathway. (2014) Rizzuti D, Ang M, Sokollik C, Wu T, Abdullah M, Greenfield L, Fattouh R, Reardon C, Tang M, Schindler C, Cattral M, Jones NL. Journal of Innate Immunity, accepted for publication.

The protein ATG16L1 suppresses inflammatory cytokines induced by the intracellular sensors Nod1 and Nod2 in an autophagy-independent manner. (2013) Sorbara MT, Ellison LK, Ramjeet M, Travassos LH, Jones NL, Girardin SE, Philpott DJ.
Immunity. 39(5):858-873.

Crohn disease ATG16L1 polymorphism increases susceptibility to infection with Helicobacter pylori in humans. (2012) Raju D, Hussey S, Jones NL. Autophagy. 8(9):1387-1388.

Vacuolating cytotoxin and variants in Atg16L1 that disrupt autophagy promote Helicobacter pylori infection in humans. (2012) Raju D, Hussey S, Ang M, Terebiznik MR, Sibony M, Galindo-Mata E, Gupta V, Blanke SR, Delgado A, Romero-Gallo J, Ramjeet MS, Mascarenhas H, Peek RM, Correa P, Streutker C, Hold G, Kunstmann E, Yoshimori T, Silverberg MS, Girardin SE, Philpott DJ, El Omar E, Jones NL.
Gastroenterology. 142(5):1160-1171.

Evidence-based guidelines from ESPGHAN and NASPGHAN for Helicobacter pylori infection in children. (2011) Koletzko S, Jones NL, Goodman KJ, Gold B, Rowland M, Cadranel S, Chong S, Colletti RB, Casswall T, Elitsur Y, Guarner J, Kalach N, Madrazo A, Megraud F, Oderda G; H pylori Working Groups of ESPGHAN and NASPGHAN. Journal of Pediatric Gastroenterology and Nutrition. 53(2):230-243.

Nod1 and Nod2 direct autophagy by recruiting ATG16L1 to the plasma membrane at the site of bacterial entry. (2010) Travassos LH, Carneiro LA, Ramjeet M, Hussey S, Kim YG, Magalhães JG, Yuan L, Soares F, Chea E, Le Bourhis L, Boneca IG, Allaoui A, Jones NL, Nuñez G, Girardin SE, Philpott DJ.
Nature Immunology. 11(1):55-62.

Effect of Helicobacter pylori's vacuolating cytotoxin on the autophagy pathway in gastric epithelial cells. (2009) Terebiznik MR, Raju D, Vázquez CL, Torbricki K, Kulkarni R, Blanke SR, Yoshimori T, Colombo MI, Jones NL. Autophagy. 5(3):370-379.

Helicobacter pylori cytotoxin-associated gene A activates the signal transducer and activator of transcription 3 pathway in vitro and in vivo. (2009) Bronte-Tinkew DM, Terebiznik M, Franco A, Ang M, Ahn D, Mimuro H, Sasakawa C, Ropeleski MJ, Peek RM Jr, Jones NL.
Cancer Research. 69(2):632-639.

Invited Reviews & Book Chapters

Wu T, Jones NL. Helicobacter pylori infection and autophagy: a paradigm for host-microbe interactions. In: AUTOPHAGY: Cancer, Other Pathologies, Inflammation, Immunity, Infection and Aging, Volume 2 (Hayat MA, eds). Academic Press, San Diego, CA. 2013: pp 211-223.

Hussey S, Jones NL. Helicobacter pylori in childhood. In: Pediatric Gastrointestinal Diseases and Liver Disease, fourth edition (Wyllie R, Hyams JS, Kay M, eds).  Elsevier Saunders, Philadelphia. 2011: pp 293-308.

Wine E, Terebiznik M, Jones NL. Microbial interactions with gut epithelium. In: Pediatric Gastrointestinal Disease, fifth edition (Kleinman, Goulet, Mieli-Vergani, Sanderson, Sherman, Schneider, eds.). BC Decker, Hamilton, ON. 2008: pp 373-390.

Walters T, Jones NL. Helicobacter pylori infection. In:  Pediatric Gastrointestinal Diseases, second edition (Wyllie R, Hyams JS, eds).  W.B. Saunders Company, Philadelphia, PA. 2008: pp 101-158.