Detection of O2− generation and neutrophil accumulation in rat lungs after acute necrotizing pancreatitis

Murakami, Hiroya; Nakao, Akimasa; Kishimoto, Wakahiko; Nakano, Masahiro; Takagi, Hiroshi

doi:10.1016/s0039-6060(05)80372-1

Cited by 56 publications

(36 citation statements)

References 21 publications

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“…This complex immune response to trauma is characterized by the release of several inflammatory mediators including IL-8, IL-1β, IL-10 and IL-18 but also neutrophil migration into the lung [13,[48][49][50][51][52][53]. Persistent accumulation of neutrophils in the lung has been linked to pulmonary damage and poor survival via an interstitial inflammation, increase of interstitial space and limitation of the oxygen transport [9][10][11][12]. In line with these reports, in the present study, we can show for the first time in a porcine animal model, that the traumainduced lung injury (depicted by increased LIS, Fig.…”

Section: Discussionmentioning

confidence: 99%

“…PMN migrate after their systemic activation by e.g. interleukin (IL)−8 into the pulmonary interstitium, release proteolytic enzymes and induce microvascular damage and harmful airway remodeling in lung tissue, which is associated with poor survival [9][10][11][12]. Moreover, the generation of inflammatory mediators including interleukin IL-8 plays an important role in ARDS pathophysiology [13][14][15][16].…”

Section: Introductionmentioning

confidence: 99%

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Leukotriene B4 indicates lung injury and on-going inflammatory changes after severe trauma in a porcine long-term model

Störmann

Auner

Schimunek

et al. 2017

Prostaglandins, Leukotrienes and Essential Fatty Acids

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A B S T R A C TBackground: Recognizing patients at risk for pulmonary complications (PC) is of high clinical relevance. Migration of polymorphonuclear leukocytes (PMN) to inflammatory sites plays an important role in PC, and is tightly regulated by specific chemokines including interleukin (IL)−8 and other mediators such as leukotriene (LT)B4. Previously, we have reported that LTB4 indicated early patients at risk for PC after trauma. Here, the relevance of LTB4 to indicating lung integrity in a newly established long-term porcine severe trauma model (polytrauma, PT) was explored. Methods: Twelve pigs (3 months old, 30 ± 5 kg) underwent PT including standardized femur fracture, lung contusion, liver laceration, hemorrhagic shock, subsequent resuscitation and surgical fracture fixation. Six animals served as controls (sham). After 72 h lung damage and inflammatory changes were assessed. LTB4 was determined in plasma before the experiment, immediately after trauma, and after 2, 4, 24 or 72 h. Bronchoalveolar lavage (BAL)-fluid was collected prior and after the experiment. Results: Lung injury, local gene expression of IL-8, IL-1β, IL-10, IL-18 and PMN-infiltration into lungs increased significantly in PT compared with sham. Systemic LTB4 increased markedly in both groups 4 h after trauma. Compared with declined plasma LTB4 levels in sham, LTB4 increased further in PT after 72 h. Similar increase was observed in BAL-fluid after PT. Conclusions: In a severe trauma model, sustained changes in terms of lung injury and inflammation are determined at day 3 post-trauma. Specifically, increased LTB4 in this porcine long-term model indicated a rapid inflammatory alteration both locally and systemically. The results support the concept of LTB4 as a biomarker for PC after severe trauma and lung contusion.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Leukotriene B4 indicates lung injury and on-going inflammatory changes after severe trauma in a porcine long-term model

Störmann

Auner

Schimunek

et al. 2017

Prostaglandins, Leukotrienes and Essential Fatty Acids

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“…Although the mechanisms underlying these processes remain incompletely understood, the morphological and functional changes include sequestration of inflammatory cells within the lung (2,7,37), injury to the pulmonary microvascular surface (19), and extravasation of otherwise intravascular fluid across the microvascular endothelial barrier into the bronchoalveolar space (21). Acute lung injury and ARDS, along with other elements of SIRS, are frequently noted in patients with severe acute pancreatitis (30).…”

mentioning

confidence: 99%

In vivo evidence for the role of GM-CSF as a mediator in acute pancreatitis-associated lung injury

Frossard

Saluja²,

Mach

et al. 2002

American Journal of Physiology-Lung Cellular and Molecular Phys

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Severe pancreatitis is frequently associated with acute lung injury (ALI) and the respiratory distress syndrome. The role of granulocyte-macrophage colony-stimulating factor (GM-CSF) in mediating the ALI associated with secretagogue-induced experimental pancreatitis was evaluated with GM-CSF knockout mice (GM-CSF −/−). Pancreatitis was induced by hourly (12×) intraperitoneal injection of a supramaximally stimulating dose of the cholecystokinin analog caerulein. The resulting pancreatitis was similar in GM-CSF-sufficient (GM-CSF +/+) control animals and GM-CSF −/− mice. Lung injury, quantitated by measuring lung myeloperoxidase activity (an indicator of neutrophil sequestration), alveolar-capillary permeability, and alveolar membrane thickness was less severe in GM-CSF −/− than in GM-CSF +/+ mice. In GM-CSF +/+ mice, pancreas, lung and serum GM-CSF levels increase during pancreatitis. Lung levels of macrophage inflammatory protein (MIP)-2 are also increased during pancreatitis, but, in this case, the rise is less profound in GM-CSF −/− mice than in GM-CSF +/+ controls. Administration of anti-MIP-2 antibodies was found to reduce the severity of pancreatitis-associated ALI. Our findings indicate that GM-CSF plays a critical role in coupling pancreatitis to ALI and suggest that GM-CSF may act indirectly by regulating the release of other proinflammatory factors including MIP-2.

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“…Weidenhach et al reported that animals with pancreatitis die due to multi-organ failures through the development of systemic inflammatory response to pancreatic injury by the activation of various enzymes, cytokines, and vasoactive substances (36). Acute lung injury and acute respiratory distress syndrome (ARDS) often occurs in the early stage of severe pancreatitis and may be related to early death (27,28). The production ofROS by the activated leukocytes resulting in increased capillary permeability plays a major role in the pathogenesis ofARDS (28).…”

Section: Discussionmentioning

confidence: 99%

“…The production ofROS by the activated leukocytes resulting in increased capillary permeability plays a major role in the pathogenesis ofARDS (28). We used LDH level in BAL fluid for the assessment of capillary permeability (28). The induction ofANP resulted in increased LDH in BAL fluid, decreased pOz and increased activities of MPO and MDA in lung tissue.…”

Section: Discussionmentioning

confidence: 99%

Effects of 17ß-Estradiol on the Acute Necrotizing Pancreatitis after Onset in Rats

et al. 2013

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The aim of this study was to investigate the influence of 178-estradiol (E 2 ) on acute necrotizing pancreatitis (ANP) induced by glycodeoxycholic acid in rats. Rats were divided into six groups as sham + saline, sham + single dose E 2 (SDE z)' sham + multiple dose E, (MDE z), ANP + saline, ANP + SDE z' and ANP + MDE z. ANP in rats was induced by glycodeoxycholic acid. The extent of acinar cell injury, mortality, systemic cardiorespiratory variables, functional capillary density (FCD), renal/hepatic functions, and changes in some enzyme markers for pancreatic and lung tissue were investigated during ANP in rats. The induction of ANP resulted in a significant increase in the mortality rate, pancreatic necrosis, and serum activity of amylase, alanine aminotransferase (ALT), interleukin (IL)-6, lactate dehydrogenase (LDU) in bronchoalveolar lavage (BAL) fluid, serum concentration of urea, and tissue activity of myeloperoxidase (MPO) and malondialdehyde (MDA) in the pancreas and lung, and a significant decrease in concentrations of calcium, blood pressure, urine output, pOz' and functional capillary density (FCD). The use of E, did not alter these changes. E, demonstrated no effect on the course of ANP in rats. Therefore, it has no value in the treatment during acute pancreatitis.

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Detection of O2− generation and neutrophil accumulation in rat lungs after acute necrotizing pancreatitis

Cited by 56 publications

References 21 publications

Leukotriene B4 indicates lung injury and on-going inflammatory changes after severe trauma in a porcine long-term model

Leukotriene B4 indicates lung injury and on-going inflammatory changes after severe trauma in a porcine long-term model

In vivo evidence for the role of GM-CSF as a mediator in acute pancreatitis-associated lung injury

Effects of 17ß-Estradiol on the Acute Necrotizing Pancreatitis after Onset in Rats

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