Evidence of a central role for p38 map kinase induction of tumor necrosis factor [alpha ] in pancreatitis-associated pulmonary injury

Yang, Jing; Murphy, Colleen; Denham, Woody; Botchkina, Galina I.; Tracey, Kevin J.; Norman, James

doi:10.1067/msy.1999.98753

Cited by 27 publications

(48 citation statements)

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“…Norman et al [7] found in SAP rats a positive correlation between the TNF-α concentrations in pancreatic tissue and plasma and the level of pancreatic injury and inflammation, which is consistent to the fact that in this experiment, the pancreas pathological score was positively correlated with TNF-α at 12 h in model group (P < 0.05). It was found in this experiment that the serum TNF-α contents were lower …”

Section: Discussionsupporting

confidence: 74%

“…TNF-α can increase the local tissue damage and capillary permeability, eventually aggravating pancreatic necrosis, which is important in AP [7,8] . Norman et al [7] found in SAP rats a positive correlation between the TNF-α concentrations in pancreatic tissue and plasma and the level of pancreatic injury and inflammation, which is consistent to the fact that in this experiment, the pancreas pathological score was positively correlated with TNF-α at 12 h in model group (P < 0.05).…”

Section: Discussionmentioning

confidence: 99%

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Effects of large dose of dexamethasone on inflammatory mediators and pancreatic cell apoptosis of rats with severe acute pancreatitis

Zhang

Chen²,

Hu³

et al. 2007

WJG

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AIM:To investigate the influence of high dose of dexamethasone on inflammatory mediators and apoptosis of rats with severe acute pancreatitis (SAP).METHODS: SAP rats were randomly assigned to the model group and treatment group while the normal rats were assigned to the sham operation group. The mortality, ascite volumes, ascites/body weight ratio and pancreas pathological changes of all rats were observed at 3, 6 and 12 h after operation. Their contents of amylase and endotoxin in plasma and contents of tumor necrosis factor (TNF-α), phospholipase A2 (PLA2) and IL-6 in serum were also determined. The microarray sections of their pancreatic tissues were prepared, terminal transferase dUTP nick end labeling (TUNEL) staining was performed and apoptotic indexes were calculated. RESULTS:There was no marked difference between treatment group and model group in survival. The contents of amylase and endotoxin in plasma and contents of TNF-α, PLA2 and IL-6 in serum, ascite volumes, ascites/body weight ratio and pancreas pathological scores were all lower in treatment group than in model group to different extents at different time

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Section: Discussionsupporting

confidence: 74%

Section: Discussionmentioning

confidence: 99%

Effects of large dose of dexamethasone on inflammatory mediators and pancreatic cell apoptosis of rats with severe acute pancreatitis

Zhang

Chen²,

Hu³

et al. 2007

WJG

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“…Inhibition of p38 MAPK decreases LPSinduced neutrophil influx, release of cytokines in the airspaces or serum, and expression of matrix metalloproteinase-9 in the airspaces (12,49,50). In two murine models of pancreatitis-induced lung injury, pretreatment with a p38 MAPK inhibitor reduced TNF-␣ release in the airways and reduced leukocyte accumulation, serum nitrites, and pulmonary edema (51,52). In an ischemia and reperfusion model of pulmonary injury, a p38 MAPK inhibitor decreased serum cytokine release and lung damage, but improved oxygenation (53).…”

Section: Discussionmentioning

confidence: 99%

Selective Suppression of Neutrophil Accumulation in Ongoing Pulmonary Inflammation by Systemic Inhibition of p38 Mitogen-Activated Protein Kinase

Nick

Young

Arndt

et al. 2002

The Journal of Immunology

105

109

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The p38 mitogen-activated protein kinase (MAPK) signaling pathway regulates a wide range of inflammatory responses in many different cells. Inhibition of p38 MAPK before exposing a cell to stress stimuli has profound anti-inflammatory effects, but little is known about the effects of p38 MAPK inhibition on ongoing inflammatory responses. LPS-induced activation of p38 MAPK in human neutrophils was inhibited by poststimulation exposure to a p38 MAPK inhibitor (M39). Release of TNF-α, macrophage-inflammatory protein (MIP)-2 (MIP-1β), and IL-8 by LPS-stimulated neutrophils was also reduced by poststimulation p38 MAPK inhibition. In contrast, release of monocyte chemoattractant protein-1 was found to be p38 MAPK independent. Ongoing chemotaxis toward IL-8 was eliminated by p38 MAPK inhibition, although the rate of nondirectional movement was not reduced. A murine model of acute LPS-induced lung inflammation was used to study the effect of p38 MAPK inhibition in ongoing pulmonary inflammation. Initial pulmonary cell responses occur within 4 h of stimulation in this model, so M39 was administered 4 h or 12 h after exposure of the animals to aerosolized LPS to avoid inhibition of cytokine release. Quantities of TNF-α, MIP-2, KC, or monocyte chemoattractant protein-1 recovered from bronchial alveolar lavage or serum were not changed. Recruitment of neutrophils, but not other leukocytes, to the airspaces was significantly reduced. Together, these data demonstrate the selective reduction of LPS-induced neutrophil recruitment to the airspaces, independent of suppression of other inflammatory responses. These findings support the feasibility of p38 MAPK inhibition as a selective intervention to reduce neutrophilic inflammation.

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“…These results are consistent with previous research which demonstrated that administration of specific TNF-α and IL-1β inhibitors prevents I/R-related remote organ injury [22][23][24][25][26][27] . Furthermore, there is good evidence that agents which decrease distant lung injury after I/R also decrease pulmonary TNF-α 20,28,29 . As the specific objective of this study was to compare lung damage between groups subjected to normothermic and hypothermic renal ischemia, it was decided that the absence of a sham group would not affect analysis or interpretation of results.…”

Section: Discussionmentioning

confidence: 99%

Analysis of the effects of topical renal hypothermia on lung tissue after kidney ischemia and reperfusion in rats

et al. 2015

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PURPOSE:To evaluate whether topical renal hypothermia (TRH) at different levels of temperature has protective effects on lung tissue after renal I/R, through an analysis of organ histology and inflammatory markers in lung tissue. METHODS:Twenty-eight male Wistar rats were randomly allocated across four groups and subjected to renal ischemia at different levels of topical renal temperature: normothermia (no cooling, 37°C), mild hypothermia (26°C), moderate hypothermia (15°C), and deep hypothermia (4°C). To induce I/R, the vessels supplying the left kidney of each animal were clamped for 40 minutes, followed by reperfusion. After four hours, another procedure was performed to harvest the tissues of interest. TNF-α, IL-1β and myeloperoxidase activity were measured in lung tissue. Histological analysis was performed in hematoxylin and eosin-stained lung specimens. RESULTS:Induction of renal I/R under deep topical hypothermia resulted in a significant decrease in lung concentrations of TNF-α compared with normothermic I/R (p<0.05). A trend toward significant correlation was found between lung IL-1β concentration and intensity of hypothermia p=0.055). No difference was found in myeloperoxidase activity or histologic injury between groups. CONCLUSION:Topical renal hypothermia reduces activation of the inflammatory cascade in the lung parenchyma. However, tissueprotective effects were not observed.

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Evidence of a central role for p38 map kinase induction of tumor necrosis factor [alpha ] in pancreatitis-associated pulmonary injury

Abstract: p38 MAP kinase-induced TNF alpha production plays a central role in the development of pulmonary dysfunction, which accompanies severe acute pancreatitis in this rodent model.

Cited by 27 publications

References 0 publications

Effects of large dose of dexamethasone on inflammatory mediators and pancreatic cell apoptosis of rats with severe acute pancreatitis

Effects of large dose of dexamethasone on inflammatory mediators and pancreatic cell apoptosis of rats with severe acute pancreatitis

Selective Suppression of Neutrophil Accumulation in Ongoing Pulmonary Inflammation by Systemic Inhibition of p38 Mitogen-Activated Protein Kinase

Analysis of the effects of topical renal hypothermia on lung tissue after kidney ischemia and reperfusion in rats

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