Controversial role of toll-like receptors in acute pancreatitis

被引:68
作者
Vaz, Juan [1 ]
Akbarshahi, Hamid [1 ]
Andersson, Roland [1 ]
机构
[1] Lund Univ, Skane Univ Hosp, Dept Surg, SE-22185 Lund, Sweden
关键词
Acute pancreatitis; Severe acute pancreatitis; Pathophysiological mechanism; Toll-like receptors; Intervention; ACUTE LUNG INJURY; FACTOR-KAPPA-B; CERULEIN-INDUCED PANCREATITIS; INFLAMMATORY RESPONSE SYNDROME; RESPIRATORY-DISTRESS-SYNDROME; MIGRATION INHIBITORY FACTOR; MESSENGER-RNA EXPRESSION; KINASE-C-ZETA; HEPARAN-SULFATE; NECROTIZING PANCREATITIS;
D O I
10.3748/wjg.v19.i5.616
中图分类号
R57 [消化系及腹部疾病];
学科分类号
100201 [内科学];
摘要
Acute pancreatitis (AP) is a common clinical condition with an incidence of about 300 or more patients per million annually. About 10%-15% of patients will develop severe acute pancreatitis (SAP) and of those, 10%-30% may die due to SAP-associated complications. Despite the improvements done in the diagnosis and management of AP, the mortality rate has not significantly declined during the last decades. Toll-like receptors (TLRs) are pattern-recognition receptors that seem to play a major role in the development of numerous diseases, which make these molecules attractive as potential therapeutic targets. TLRs are involved in the development of the systemic inflammatory response syndrome, a potentially lethal complication in SAP. In the present review, we explore the current knowledge about the role of different TLRs that have been described associated with AP. The main candidate for targeting seems to be TLR4, which recognizes numerous damage-associated molecular patterns related to AP. TLR2 has also been linked with AP, but there are only limited studies that exclusively studied its role in AP. There is also data suggesting that TLR9 may play a role in AP. (C) 2013 Baishideng. All rights reserved.
引用
收藏
页码:616 / 630
页数:15
相关论文
共 127 条
[1]
CD44 Participates in IP-10 Induction in Cells in Which Hepatitis C Virus RNA Is Replicating, through an Interaction with Toll-Like Receptor 2 and Hyaluronan [J].
Abe, Takayuki ;
Fukuhara, Takasuke ;
Wen, Xiauyu ;
Ninomiya, Akinori ;
Moriishi, Kohji ;
Maehara, Yoshihiko ;
Takeuchi, Osamu ;
Kawai, Taro ;
Akira, Shizuo ;
Matsuura, Yoshiharu .
JOURNAL OF VIROLOGY, 2012, 86 (11) :6159-6170
[2]
Nuclear factor-κB and its role in sepsis-associated organ failure [J].
Abraham, E .
JOURNAL OF INFECTIOUS DISEASES, 2003, 187 :S364-S369
[3]
TLR4 dependent heparan sulphate-induced pancreatic inflammatory response is IRF3-mediated [J].
Akbarshahi, Hamid ;
Axelsson, Jakob B. F. ;
Said, Katarzyna ;
Malmstrom, Anders ;
Fischer, Hans ;
Andersson, Roland .
JOURNAL OF TRANSLATIONAL MEDICINE, 2011, 9
[4]
Toll-like receptors: critical proteins linking innate and acquired immunity [J].
Akira, S ;
Takeda, K ;
Kaisho, T .
NATURE IMMUNOLOGY, 2001, 2 (08) :675-680
[5]
Toll-like receptor signalling [J].
Akira, S ;
Takeda, K .
NATURE REVIEWS IMMUNOLOGY, 2004, 4 (07) :499-511
[6]
Signaling danger:: Toll-like receptors and their potential roles in kidney disease [J].
Anders, HJ ;
Banas, B ;
Schlöndorff, D .
JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY, 2004, 15 (04) :854-867
[7]
Incidence, management and recurrence rate of acute pancreatitis [J].
Andersson, R ;
Andersson, B ;
Haraldsen, P ;
Drewsen, G ;
Eckerwall, G .
SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY, 2004, 39 (09) :891-894
[8]
Incidence, aetiology and mortality rate of acute pancreatitis over 10 years in a defined urban population in Sweden [J].
Appelros, S ;
Borgström, A .
BRITISH JOURNAL OF SURGERY, 1999, 86 (04) :465-470
[9]
TLR4 mutations are associated with endotoxin hyporesponsiveness in humans [J].
Arbour, NC ;
Lorenz, E ;
Schutte, BC ;
Zabner, J ;
Kline, JN ;
Jones, M ;
Frees, K ;
Watt, JL ;
Schwartz, DA .
NATURE GENETICS, 2000, 25 (02) :187-+
[10]
Novel signal transduction pathway utilized by extracellular HSP70 -: Role of Toll-like receptor (TLR) 2 AND TLR4 [J].
Asea, A ;
Rehli, M ;
Kabingu, E ;
Boch, JA ;
Baré, O ;
Auron, PE ;
Stevenson, MA ;
Calderwood, SK .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2002, 277 (17) :15028-15034