Relationship between pancreatitis and lung diseases

被引:76
作者
Steer, ML [1 ]
机构
[1] Harvard Univ, Sch Med, Boston, MA 02215 USA
[2] Beth Israel Deaconess Med Ctr, Boston, MA 02215 USA
来源
RESPIRATION PHYSIOLOGY | 2001年 / 128卷 / 01期
关键词
D O I
10.1016/S0034-5687(01)00259-6
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Patients with acute pancreatitis may develop acute lung injury, manifest clinically as the adult respiratory distress syndrome. Most patients who die during the early stages of severe acute pancreatitis die either with or as a result of this lung injury. To explore the events which couple acute pancreatitis to lung injury, a number of recent studies have been performed in the author's laboratory using a variety of experimental models and interventions including gene-targeted deletion of chemokines, cytokines, specific receptors, and adhesion molecules. These studies have indicated that adhesion molecules such as intracellular adhesion molecule-1 (ICAM-1), neutrophils, platelet activating factor (PAF), substance P, and chemokines acting via the CCR-1 chemokine receptor play a pro-inflammatory role while complement factor C5a plays an anti-inflammatory role in pancreatitis and lung injury. Future studies will build on these observations to expand the list of pro- and anti-inflammatory coupling factors and explore the mechanisms by which they act to cause or prevent lung injury in acute pancreatitis. (C) 2001 Elsevier Science BN. All rights reserved.
引用
收藏
页码:13 / 16
页数:4
相关论文
共 13 条
[1]   Role of substance P and the neurokinin 1 receptor in acute pancreatitis and pancreatitis-associated lung injury [J].
Bhatia, M ;
Saluja, AK ;
Hofbauer, B ;
Frossard, JL ;
Lee, HS ;
Castagliuolo, I ;
Wang, CC ;
Gerard, N ;
Pothoulakis, C ;
Steer, ML .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1998, 95 (08) :4760-4765
[2]  
Bhatia M, 1998, INT J PANCREATOL, V24, P77
[3]  
Bhatia M., 1997, Pancreas, V15, P428
[4]   The role of intercellular adhesion molecule 1 and neutrophils in acute pancreatitis and pancreatitis-associated lung injury [J].
Frossard, JL ;
Saluja, A ;
Bhagat, L ;
Lee, HS ;
Bhatia, M ;
Hofbauer, B ;
Steer, ML .
GASTROENTEROLOGY, 1999, 116 (03) :694-701
[5]   Targeted disruption of the beta-chemokine receptor CCR1 protects against pancreatitis-associated lung injury [J].
Gerard, C ;
Frossard, JL ;
Bhatia, M ;
Saluja, A ;
Gerard, NP ;
Lu, B ;
Steer, M .
JOURNAL OF CLINICAL INVESTIGATION, 1997, 100 (08) :2022-2027
[6]   NEUTROPHIL-DEPENDENT, OXYGEN-RADICAL MEDIATED LUNG INJURY ASSOCIATED WITH ACUTE-PANCREATITIS [J].
GUICE, KS ;
OLDHAM, KT ;
CATY, MG ;
JOHNSON, KJ ;
WARD, PA .
ANNALS OF SURGERY, 1989, 210 (06) :740-747
[7]   PANCREATITIS-INDUCED ACUTE LUNG INJURY - AN ARDS MODEL [J].
GUICE, KS ;
OLDHAM, KT ;
JOHNSON, KJ ;
KUNKEL, RG ;
MORGANROTH, ML ;
WARD, PA .
ANNALS OF SURGERY, 1988, 208 (01) :71-77
[8]   Effect of recombinant platelet-activating factor acetylhydrolase on two models of experimental acute pancreatitis [J].
Hofbauer, B ;
Saluja, AK ;
Bhatia, M ;
Frossard, JL ;
Lee, HS ;
Bhagat, L ;
Steer, ML .
GASTROENTEROLOGY, 1998, 115 (05) :1238-1247
[9]  
Jaffray C, 2000, GASTROENTEROLOGY, V118, pA167
[10]  
LAMPEL M, 1977, VIRCHOWS ARCH A, V373, P107