The Authors' reply
- Aleixo M Muise1,2,3,
- Ramzi Fattouh2,
- Grace Y Lam2,
- Sandeep Dhillon2,3,
- John H Brumell2,3,4
- 1Division of Gastroenterology, Hepatology, and Nutrition, Department of Paediatrics, Hospital for Sick Children, Toronto, Ontario, Canada
- 2Program in Cell Biology, the Hospital for Sick Children and University of Toronto, Toronto, Ontario, Canada
- 3Institute of Medical Science, University of Toronto, Toronto, Ontario, Canada
- 4Department of Molecular Genetics, University of Toronto, Toronto, Ontario, Canada
- Correspondence to Dr Aleixo Muise, Division of Gastroenterology, Program in Cell Biology, Hospital for Sick Children, 555 University Ave, Toronto, ON M5G 1X8, Canada; aleixo.muise{at}utoronto.ca
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Contributors All authors contributed equally to this letter.
- IBD, inflammatory bowel disease
- Crohn's diseaseChronic Granulomatous disease
- Chronic Granulomatous disease
- reactive oxygen species
- NADPH oxidase complex
- IBD - genetics
- IBD basic research
- IBD clinical
- bacterial pathogenesis
- cell biology
- cellular immunity
- salmonella
We read with interest the letter by Somasundaram et al1 in response to our paper ‘NADPH oxidase complex and IBD candidate gene studies: identification of a rare variant in NCF2 that results in reduced binding to RAC2’ that further demonstrates the importance of the NADPH oxidase complex genes in the pathogenesis of Crohn's disease. Their letter provides interesting confirmatory data that complement our findings, which already clearly demonstrate the role of the NADPH oxidase complex in inflammatory bowel disease (IBD).2 However, there are a number of important issues that require further clarification.
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Somasundaram et al suggest that our study did not show the association between reactive oxygen species (ROS) production and IBD.1 Our study clearly shows that ROS production is important …
