Original communicationEarly complement system activation and neutrophil priming in acute pancreatitis: Participation of trypsin☆
References (38)
Time-dependent alterations in the deformability of human neutrophils in response to chemotactic activation
Blood
(1990)- et al.
Is fatal pancreatitis a consequence of excessive leukocyte stimulation? the role of tumor necrosis factor alpha
Cytokine
(1991) - et al.
Amelioration of the physiologic and biochemical changes of acute pancreatitis using anti-TNF-alpha polyclonal antibody
Am J Surg
(1994) - et al.
Interleukin-8 and development of adult respiratory distress syndrome in at risk patient groups
Lancet
(1993) - et al.
Elevation of serum interleukin-6 concentration precedes acute phase response and reflects severity in acute pancreatitis
Gastroenterology
(1991) - et al.
Myeloperoxidase of the leukocyte of normal human blood. 1. content and localization
Arch Biochem Biophys
(1962) - et al.
The NADPH oxidase of human polymorphonuclear leukocytes: evidence for regulation by multiple signals
J Biol Chem
(1984) - et al.
Activation of human neutrophils by C3a and C5a: comparison of the effects on shape changes, chemotaxis, secretion, and respiratory burst
FEBS Letter
(1994) - et al.
Death due to acute pancreatitis: a retrospective analysis of 405 autopsy cases
Dig Dis Sci
(1985) - et al.
Neutrophils and the adult respiratory distress syndrome
Am Rev Respir Dis
(1983)
Lung neutrophils in the adult respiratory distress syndrome: clinical and pathophysiological significance
Am Rev Respir Dis
Mechanics of stimulated neutrophils: cell stiffening induces retention in capillaries
Science
Mechanisms of lipopolysaccharide-induced neutrophil retention: relative contributions of adhesive and cellular mechanical properties
J Immunol
Endotoxaemia and serum tumor necrosis factor as prognostic factors in severe acute pancreatitis
Gut
Induction of tumor necrosis factor in severe acute pancreatitis and its subsequent reduction after hepatic passage
Surgery
Inflammatory mediators in acute pancreatitis
Br J Surg
The role of tumor necrosis factor alpha in the aggravation of cerulein-induced pancreatitis in rats
Int J Pancreatol
Inflammatory mediators and cytokines: new aspects of the pathophysiology and assessment of severity of acute pancreatitis?
Hepatogastroenterology
Interleukin-8 and neutrophil activation in acute pancreatitis
Eur J Clin Invest
Cited by (43)
Proteomic analysis of therapeutic effects of Qingyi pellet on rodent severe acute pancreatitis-associated lung injury
2019, Biomedicine and PharmacotherapyCitation Excerpt :Macrophage polarization and neutrophil accumulation are major causes in SAP-ALI [6–9]. Pancreatin, especially phospholipase A2, complement system and nuclear factor kappa-B (NF-kB) are also key factors during the process of SAP-ALI [10–12]. Cytokine cascade amplification, oxidative stress reaction and related apoptosis are closely related to the development of SAP-ALI [13–15].
Controlling the anaphylatoxin C5a in diseases requires a specifically targeted inhibition
2017, Clinical ImmunologyCitation Excerpt :In patients with multiple trauma, the activated factor VII-activating protease (FSAP) and the pro-apoptotic aspartic protease cathepsin D were able to directly trigger C5a generation and thereby contributed to the posttraumatic inflammatory response in vivo [23,24]. In addition, trypsin was described as potential trigger of complement activation leading to C3a and C5a production in the experimental setting of acute pancreatitis [25]. Interestingly, several proteases produced by the anaerobic bacterium Porphyromonas gingivalis were capable of degrading complement C5, resulting in the production of biologically active C5a [26].
Complement Component 5 Mediates Development of Fibrosis, via Activation of Stellate Cells, in 2 Mouse Models of Chronic Pancreatitis
2015, GastroenterologyCitation Excerpt :This suggests a similar pathophysiological mechanism behind the profibrotic function of C5a in liver disease and pancreatitis. Activation of the complement system by pancreatic proteases such as trypsin16,40 may start recovery from pancreatic necrosis by induction of fibrosis through activating PSCs. Whether or not variants of the human C5 gene represent risk factors for fibrotic disease has been discussed controversially.
Increased expression of the intercellular adhesion molecule-1 (ICAM-1) on peripheral blood neutrophils in acute pancreatitis
2014, Advances in Medical SciencesCitation Excerpt :These mediators are being considered as major elements responsible for transformation of local inflammatory response within the pancreas into systemic inflammatory response syndrome (SIRS) which overwhelms compensatory anti-inflammatory response syndrome (CARS) and eventually leads to multiorgan failure (MOF) [6–8]. Previous studies have suggested that AP is frequently associated with sequestration of inflammatory cells, particularly neutrophils, within pancreas, and it is generally believed to be an early and important event in the evolution of pancreatitis [9]. The aim of our study was to evaluate parameters of peripheral neutrophils activation, focused on the expression of adhesion molecules, in patients with AP.
Oxygen in the alveolar air space mediates lung inflammation in acute pancreatitis
2004, Free Radical Biology and Medicine
- ☆
Supported by grant-in-aid from the Ministry of Education, Science and Culture of Japan.