CD40L is not involved in acute experimental pancreatitis
Abdulla, Aree LU ; Awla, Darbaz LU ; Jeppsson, Bengt LU ; Regnér, Sara LU
and Thorlacius, Henrik
LU
(2011)
In European Journal of Pharmacology
659(1).
p.85-88
- Abstract
- Recent data suggest that platelets not only control thrombosis and hemostasis but may also regulate inflammatory processes such as acute pancreatitis. However, the specific role of platelet-derived mediators in the pathophysiology of acute pancreatitis is not known. Herein, we examined the role of CD40 ligand (CD40L, CD154) in different models of acute pancreatitis. Acute pancreatitis was induced by repetitive caerulein administration (50 mu g/kg, i.p.) or infusion of sodium taurocholate (5%-10 mu l) into the pancreatic duct in wild-type C578L/6 and CD40L-deficient mice. Neutrophil infiltration, myeloperoxidase (MPO), macrophage inflammatory protein-2 (MIP-2) levels, acinar cell necrosis, edema and hemorrhage in the pancreas as well as... (More)
- Recent data suggest that platelets not only control thrombosis and hemostasis but may also regulate inflammatory processes such as acute pancreatitis. However, the specific role of platelet-derived mediators in the pathophysiology of acute pancreatitis is not known. Herein, we examined the role of CD40 ligand (CD40L, CD154) in different models of acute pancreatitis. Acute pancreatitis was induced by repetitive caerulein administration (50 mu g/kg, i.p.) or infusion of sodium taurocholate (5%-10 mu l) into the pancreatic duct in wild-type C578L/6 and CD40L-deficient mice. Neutrophil infiltration, myeloperoxidase (MPO), macrophage inflammatory protein-2 (MIP-2) levels, acinar cell necrosis, edema and hemorrhage in the pancreas as well as serum amylase activity and lung levels of MPO were quantified 24 h after induction of acute pancreatitis. Caerulein and taurocholate challenge caused a clear-cut pancreatic damage characterized by increased acinar cell necrosis, neutrophil infiltration, focal hemorrhage, edema formation as well as increased levels of serum amylase and MIP-2 in the pancreas and lung MPO and histological damage. Notably, CD40L gene-deficient animals exhibited a similar phenotype as wild-type mice after challenge with caerulein and taurocholate. Similarly, administration of an antibody directed against CD40L had no effect against acute pancreatitis. Our data suggest that CD40L does not play a functional role in experimental acute pancreatitis. Thus, other candidates than CD40L needs to be explored in order to identify platelet-derived mediators in the pathophysiology of acute pancreatitis. (C) 2011 Elsevier B.V. All rights reserved. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1985485
- author
- Abdulla, Aree
LU
; Awla, Darbaz
LU
; Jeppsson, Bengt
LU
; Regnér, Sara
LU
and Thorlacius, Henrik
LU
- organization
- publishing date
- 2011
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Amylase, Chemokine, Inflammation, Neutrophil, Pancreatitis, Platelet
- in
- European Journal of Pharmacology
- volume
- 659
- issue
- 1
- pages
- 85 - 88
- publisher
- Elsevier
- external identifiers
-
- wos:000291119300013
- scopus:79958831588
- pmid:21419763
- ISSN
- 1879-0712
- DOI
- 10.1016/j.ejphar.2011.03.008
- language
- English
- LU publication?
- yes
- id
- da02d9ca-380e-402f-9a3d-f21bdf7fc323 (old id 1985485)
- date added to LUP
- 2016-04-01 10:02:22
- date last changed
- 2025-04-04 14:27:00
@article{da02d9ca-380e-402f-9a3d-f21bdf7fc323,
abstract = {{Recent data suggest that platelets not only control thrombosis and hemostasis but may also regulate inflammatory processes such as acute pancreatitis. However, the specific role of platelet-derived mediators in the pathophysiology of acute pancreatitis is not known. Herein, we examined the role of CD40 ligand (CD40L, CD154) in different models of acute pancreatitis. Acute pancreatitis was induced by repetitive caerulein administration (50 mu g/kg, i.p.) or infusion of sodium taurocholate (5%-10 mu l) into the pancreatic duct in wild-type C578L/6 and CD40L-deficient mice. Neutrophil infiltration, myeloperoxidase (MPO), macrophage inflammatory protein-2 (MIP-2) levels, acinar cell necrosis, edema and hemorrhage in the pancreas as well as serum amylase activity and lung levels of MPO were quantified 24 h after induction of acute pancreatitis. Caerulein and taurocholate challenge caused a clear-cut pancreatic damage characterized by increased acinar cell necrosis, neutrophil infiltration, focal hemorrhage, edema formation as well as increased levels of serum amylase and MIP-2 in the pancreas and lung MPO and histological damage. Notably, CD40L gene-deficient animals exhibited a similar phenotype as wild-type mice after challenge with caerulein and taurocholate. Similarly, administration of an antibody directed against CD40L had no effect against acute pancreatitis. Our data suggest that CD40L does not play a functional role in experimental acute pancreatitis. Thus, other candidates than CD40L needs to be explored in order to identify platelet-derived mediators in the pathophysiology of acute pancreatitis. (C) 2011 Elsevier B.V. All rights reserved.}},
author = {{Abdulla, Aree and Awla, Darbaz and Jeppsson, Bengt and Regnér, Sara and Thorlacius, Henrik}},
issn = {{1879-0712}},
keywords = {{Amylase; Chemokine; Inflammation; Neutrophil; Pancreatitis; Platelet}},
language = {{eng}},
number = {{1}},
pages = {{85--88}},
publisher = {{Elsevier}},
series = {{European Journal of Pharmacology}},
title = {{CD40L is not involved in acute experimental pancreatitis}},
url = {{http://dx.doi.org/10.1016/j.ejphar.2011.03.008}},
doi = {{10.1016/j.ejphar.2011.03.008}},
volume = {{659}},
year = {{2011}},
}