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World J Gastroenterol. May 21, 2014; 20(19): 5801-5807
Published online May 21, 2014. doi: 10.3748/wjg.v20.i19.5801
Published online May 21, 2014. doi: 10.3748/wjg.v20.i19.5801
Acute pancreatitis: The stress factor
Marcelo G Binker, Laura I Cosen-Binker, CBRHC Research Center, 1053 Ciudad Autónoma de Buenos Aires, Buenos Aires 1426, Argentina
Laura I Cosen-Binker, Department of Molecular and Cell Biology, Henry M Goldman School of Dental Medicine, Boston University, Boston, MA 02118, United States
Author contributions: Binker MG and Cosen-Binker LI contributed equally to this work.
Supported by KB and Associates Representing Certification International (United Kingdom) Limited
Correspondence to: Dr. Laura I Cosen-Binker, Department of Molecular and Cell Biology, Henry M Goldman School of Dental Medicine, Boston University, 72 East Concord Street - Evans Building - Room 408, Boston, MA 02118, United States. licb@bu.edu
Telephone: +1-617-4141084 Fax: +1-617-4141041
Received: February 10, 2014
Revised: March 12, 2014
Accepted: April 8, 2014
Published online: May 21, 2014
Revised: March 12, 2014
Accepted: April 8, 2014
Published online: May 21, 2014
Core Tip
Core tip: Depending on the timing and duration, stress can result in beneficial or harmful consequences. Regarding the exocrine pancreas, a previous acute-short-term stress decreases the severity of experimentally-induced pancreatitis. This protection is conferred by distinct heat shock proteins (HSP) including HSP27, HSP60 and HSP70. Conversely, chronic stress increases the susceptibility of the exocrine pancreas, aggravating pancreatitis episodes. These worsening effects are mainly mediated by tumor necrosis factor alpha.