Pawel Kiela, DVM, PhD

Contact Information:

Pediatrics, Arizona Health Sciences Center, Room 6341E
Phone: (520) 626-9687
Fax: (520) 626-4141
Email: pkiela@peds.arizona.edu

Education:

DVM--School of Veterinary Medicine, Warsaw, Poland 1994
PhD--School of Veterinary Medicine, Warsaw, Poland/Lund University, Sweden 1996

Research:

Therapeutic and pathophysiological aspects of Inflammatory Bowel Diseases
Crohn’s disease (CD) and ulcerative colitis (UC) are two spontaneously relapsing, immunologically mediated disorders of the gastrointestinal tract which are characterized by intestinal inflammation and mucosal damage. These chronic, debilitating conditions characterized by abnormal and persistent immune response to intestinal commensal flora have multifactorial etiology, with genetic predispositions and environmental factors contributing to the ultimate clinical manifestation. Despite recent advances in understanding the pathophysiology of IBD and development of new biological agents to treat active inflammation and to maintain remission, our knowledge and therapeutic options are still limited.

Our laboratory, funded by the National Institute of Diabetes and Digestive and Kidney Diseases of the NIH, studies three aspects of IBD:

Pre-clinical studies on the effectiveness and mechanism of action of curcumin (a natural non-specific inhibitor of NF-kappa-B) in mouse models of CD and UC (chemically induced colitis and spontaneous colitis in IL-10 or TCR-alpha knockout mice).
The role of NHE3, the major intestinal Na+/H+ exchanger, in the maintenance of epithelial integrity of the gut, and in modulation of the immune response in Inflammatory Bowel Diseases.
The effects of acute and chronic colitis and inflammatory mediators on key players of systemic inorganic phosphate homeostasis, and its contribution to osteopenia and osteoporosis frequently associated with IBD.

Publications:

Larmonier CB, Uno JK, Lee KM, Karrasch T, Laubitz D, Thurston R, Midura-Kiela MT, Ghishan FK, Sartor RB, Jobin C, Kiela PR. Limited Effects of Dietary Curcumin on Th-1 Driven Colitis in IL-10 Deficient Mice Suggest an IL-10 Dependent Mechanism of Protection. Am J Physiol Gastrointest Liver Physiol. Sep 25, 2008. [Epub ahead of print]
Billerey-Larmonier C, Uno JK, Larmonier N, Midura AJ, Timmermann B, Ghishan FK, Kiela PR. Protective effects of dietary curcumin in mouse model of chemically-induced colitis are strain dependent. Inflammatory Bowel Diseases 2008 Jan 15; [Epub ahead of print]
Laubitz D, Larmonier CB, Bai A, Midura-Kiela MT, Thurston R, Kiela PR, Ghishan FK. Colonic gene expression profile in NHE3-deficient mice: evidence for spontaneous distal colitis. Am J Physiol Gastrointest Liver Physiol. 2008 May 8. [Epub ahead of print]
Laubitz D, Larmonier CB, Bai A, Midura-Kiela MT, Thurston R, Kiela PR, Ghishan FK. Colonic gene expression profile in NHE3-deficient mice: evidence for spontaneous distal colitis. Am J Physiol Gastrointest Liver Physiol. 295(1):G63-G77, 2008
Billerey-Larmonier C, Uno JK, Larmonier N, Midura AJ, Timmermann B, Ghishan FK, Kiela PR. Protective effects of dietary curcumin in mouse model of chemically-induced colitis are strain dependent. Inflammatory Bowel Diseases Jun;14(6):780-93, 2008
Funk JF, Frye JB, Oyarzo JN, Kuscuoglu N, Wilson J, McCaffrey G, Stafford G, Chen G, Lantz RD, Jolad SD, Sólyom AM, Kiela PR, Timmermann BN. Efficacy and Mechanism of Action of Turmeric Supplements in the Treatment of Experimental Arthritis. Arthritis & Rheumatism, 54(11):3452-3464, 2006.

Peer-reviewed publications

Click here to see a listing of Peer-reviewed publications