Substance P-regulated leukotriene B4 production promotes acute pancreatitis-associated lung injury through neutrophil reverse migration

2018 ◽  
Vol 57 ◽  
pp. 147-156 ◽  
Author(s):  
Bin Li ◽  
Xiao Han ◽  
Xin Ye ◽  
Jianbo Ni ◽  
Jianghong Wu ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Substance P ◽  
Lung Injury ◽  
Leukotriene B4 ◽  
Reverse Migration

Preprotachykinin-A gene deletion protects mice against acute pancreatitis and associated lung injury

2003 ◽  
Vol 284 (5) ◽  
pp. G830-G836 ◽  
Author(s):  
Madhav Bhatia ◽  
John Slavin ◽  
Yuqing Cao ◽  
Allan I. Basbaum ◽  
John P. Neoptolemos
Keyword(s):  
Acute Pancreatitis ◽  
Substance P ◽  
Lung Injury ◽  
Gene Deletion ◽  
Gene Products ◽  
Nk1 Receptors ◽  
Proinflammatory Mediators ◽  
Pancreatic Damage ◽  
Impaired Lung Function ◽  
Nk2 Receptor

Impaired lung function in severe acute pancreatitis is the primary cause of morbidity and mortality in this condition. Preprotachykinin-A (PPT-A) gene products substance P and neurokinin (NK)-A have been shown to play important roles in neurogenic inflammation. Substance P acts primarily (but not exclusively) via the NK1 receptor. NKA acts primarily via the NK2 receptor. Earlier work has shown that knockout mice deficient in NK1 receptors are protected against acute pancreatitis and associated lung injury. NK1 receptors, however, bind other peptides in addition to substance P, not all of which are derived from the PPT-A gene. To examine the role of PPT-A gene products in acute pancreatitis, the effect of PPT-A gene deletion on the severity of acute pancreatitis and the associated lung injury was investigated. Deletion of PPT-A almost completely protected against acute pancreatitis-associated lung injury, with a partial protection against local pancreatic damage. These results show that PPT-A gene products are critical proinflammatory mediators in acute pancreatitis and the associated lung injury.

scholarly journals Role of substance P and the neurokinin 1 receptor in acute pancreatitis and pancreatitis-associated lung injury

1998 ◽  
Vol 95 (8) ◽  
pp. 4760-4765 ◽  
Author(s):  
M. Bhatia ◽  
A. K. Saluja ◽  
B. Hofbauer ◽  
J.-L. Frossard ◽  
H. S. Lee ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Substance P ◽  
Lung Injury ◽  
Neurokinin 1 Receptor ◽  
Neurokinin 1

scholarly journals Substance P mediates inflammatory oedema in acute pancreatitis via activation of the neurokinin-1 receptor in rats and mice

2000 ◽  
Vol 130 (3) ◽  
pp. 505-512 ◽  
Author(s):  
Eileen F Grady ◽  
Shandra K Yoshimi ◽  
John Maa ◽  
Dahlia Valeroso ◽  
Robert K Vartanian ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Substance P ◽  
Neurokinin 1 Receptor ◽  
Neurokinin 1 ◽  
Rats And Mice

Complement factor C5a exerts an anti-inflammatory effect in acute pancreatitis and associated lung injury

2001 ◽  
Vol 280 (5) ◽  
pp. G974-G978 ◽  
Author(s):  
Madhav Bhatia ◽  
Ashok K. Saluja ◽  
Vijay P. Singh ◽  
Jean-Louis Frossard ◽  
Hong-Sik Lee ◽  
...  
Keyword(s):  
Acute Pancreatitis ◽  
Lung Injury ◽  
Acute Inflammation ◽  
Complement Factor ◽  
Neutrophil Sequestration ◽  
C5a Receptors ◽  
Acinar Cell Necrosis ◽  
Anti Inflammatory ◽  
Type Strains ◽  
Inflammatory Effect

Complement factor C5a acting via C5a receptors (C5aR) is recognized as an anaphylotoxin and chemoattractant that exerts proinflammatory effects in many pathological states. The effects of C5a and C5aR in acute pancreatitis and in pancreatitis-associated lung injury were evaluated using genetically altered mice that either lack C5aR or do not express C5. Pancreatitis was induced by administration of 12 hourly injections of cerulein (50 μg/kg ip). The severity of pancreatitis was determined by measuring serum amylase, neutrophil sequestration in the pancreas, and acinar cell necrosis. The severity of lung injury was evaluated by measuring neutrophil sequestration in the lung and pulmonary microvascular permeability. In both strains of genetically altered mice, the severity of pancreatitis and pancreatitis-associated lung injury was greater than that noted in the comparison wild-type strains of C5aR- and C5-sufficient animals. This exacerbation of injury in the absence of C5a function indicates that, in pancreatitis, C5a exerts an anti-inflammatory effect. Potentially, C5a and its receptor are capable of both promoting and reducing the extent of acute inflammation.

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