Alterations of Adhesion Molecule Expression and Inflammatory Mediators in Acute Lung Injury Induced by Septic and Non-septic Challenges

Zhao, Xia; Dib, Marwan; Andersson, Ellen; Shi, Changbin; Widegren, Bengt; Wang, Xiangdong; Andersson, Roland

doi:10.1007/s00408-004-2522-3

Cited by 16 publications

(10 citation statements)

References 22 publications

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“…Absence of this molecule impairs the ability of PMN to migrate into organ tissues and reduces consequent secondary organ damage resulting in improved clinical status and overall survival. MCP-1, a chemokine was shown to act as a chemoattractant for neutrophils [7,8]. MCP-1 is known to orchestrate migration of leukocytes during sepsis leading to tissue injury.…”

Section: Discussionmentioning

confidence: 99%

“…Additionally, LPS also stimulate adhesion, activation, and infiltration of polymorphonuclear neutrophils (PMN) and damaging the alveolar-capillary membrane [6]. Intercellular adhesion molecule-1 (ICAM-1) and monocyte chemoattractant protein-1 (MCP-1) which are known to attract neutrophils [7,8] are increased in sepsis and further results in the tissue infiltration of more PMN, which in turn leads to parenchymal cell dysfunction and tissue damage [9]. Increased matrix metalloproteinases (MMPs) activity cause impairment in lung function due to decreased lung collagen content and disorganized pulmonary parenchymal tissue.…”

Section: Introductionmentioning

confidence: 99%

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Betulinic acid attenuates lung injury by modulation of inflammatory cytokine response in experimentally-induced polymicrobial sepsis in mice

et al. 2015

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Betulinic acid attenuates lung injury by modulation of inflammatory cytokine response in experimentally-induced polymicrobial sepsis in mice

et al. 2015

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“…The mechanism responsible for acute lung injury caused by SAP is quite complicated and remains unclear till now. It is now believed that pancreatin, adhension molecule, neutrophil, various inflammatory mediators, etc play extremely important roles in the onset process [28][29][30] . It has been shown an increase in expression of manifold inflammation-inducing cytokines in the lung tissue at early injury stage, while the activation of transcription factor NF-κB can stimulate the expression of manifold cytokines.…”

Section: Discussionmentioning

confidence: 99%

Influence of dexamethasone on inflammatory mediators and NF-κB expression in multiple organs of rats with severe acute pancreatitis

Zhang

Zhang²,

Chen³

et al. 2007

WJG

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A I M :To o b s e r v e t h e t h e r a p e u t i c e f f e c t s o f dexamethasone on rats with severe acute pancreatitis (SAP) and investigate the influences of dexamethasone on the inflammatory mediators and NF-κB expression in multiple organs of SAP rats as well as the mechanisms involved. METHODS:Ninety Sprague-Dawley (SD) rats with SAP were randomly divided into the model group (n = 45) and dexamethasone treatment group (n = 45), and another 45 rats were selected for the sham operation group. All groups were randomly subdivided into the 3 h, 6 h and 12 h groups, each group containing 15 rats. The survival of all groups and pathological changes of multiple organs (liver, kidney and lung) were observed at different time points after the operation. The pathological score of multiple organs was carried out, followed by the determination of amylase, endotoxin and TNF-α contents in blood. The tissue microarray was used to detect the expression levels of NF-κB p65 protein in multiple organs. RESULTS:There was no marked difference between the model group and treatment group in the survival rate. The amylase content of the treatment group was significantly lower compared to the model group at 12 h (P < 0.01, 7791.00 vs 9195.00). Moreover, the endotoxin and TNF-α levels of the treatment group were significantly lower than that of the model group at 6 h and 12 h (P < 0.01, 0.040 vs 0.055, 0.042 vs 0.059 and P < 0.05, 58.30 vs 77.54, 38.70 vs 67.30, respectively).Regarding the changes in liver NF-κB expression, the model group significantly exceeded the sham operation group at 3 h (P < 0.01, 1.00 vs 0.00), and the treatment group significantly exceeded the sham operation group at 12 h (P < 0.01, 1.00 vs 0.00), whereas no marked difference was observed between the model group and treatment group at all time points. The kidney NF-κB expression level in the treatment group significantly exceeded the model group (P < 0.05, 2.00 vs 0.00) and the sham operation group (P < 0.01, 2.00 vs 0.00) at 12 h.No NF-κB expression in the lung was found in any group. CONCLUSION:Dexamethasone can lower the amylase, endotoxin and TNF-α levels as well as mortality of SAP rats. NF-κB plays an important role in multiple organ injury. Further studies should be conducted to determine whether dexamethasone can ameliorate the pathological changes of multiple organs by reducing the NF-κB expression in the liver and kidney. The advantages of tissue microarrays in pancreatitis pathological examination include time-and energy-saving, and are highly efficient and representative. The restriction of tissue microarrays on the representation of tissues to various extents due to small diameter may lead to the deviation of analysis. treatment group was injected once with dexamethasone (1 mL = 5 mg) via the vena caudalis, 0.5 mg/100 g body weight 15 min after successful preparation of SAP model. During the laparotomy in the sham operation group, we performed pancreas and duodenum manipulation, observed pathological changes of multiple organs and fi...

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“…In contrast, plasma levels of MCP-1 increased in parallel with plasma exudation from the circulation to the alveolar space and BALF MCP-1 levels increased in parallel with plasma exudation from the circulation to the interstitial tissue. In both sepsis-and pancreatitisinduced lung injury, BALF levels of MCP-1 increased earlier than the occurrence of plasma exudation to the bronchoalveolar space (13). This supports the clinical finding that both local (intraperitoneal) and systemic levels of MCP-1 increase early during the course of severe AP in humans (28).…”

Section: Are Neutrophils Involved In Pali?mentioning

confidence: 62%

“…Comparing pancreatitis and sepsis, neutrophil infiltration into the lungs reveals two pathophysiological characteristics: (i) an increase with time after challenge; and (ii) more pronounced infiltration in pancreatitis than sepsis, demonstrating a more rapid course of disease in pancreatitis animals (13). Although neutrophils may play an important role in the development of PALI, neutrophil depletion was found to only partially reduce its severity (16), indicating that other inflammatory cells or products may contribute to PALI.…”

Section: Are Neutrophils Involved In Pali?mentioning

confidence: 97%

A new understanding of pancreatitis-associated pulmonary injury

Zhao¹,

Shi²,

Wang³

et al. 2006

Journal of Organ Dysfunction

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Pancreatitis-associated lung injury (PALI) is one of the earliest organ dysfunctions occurring in patients with severe acute pancreatitis. In this review we explore potential mechanisms of endothelial barrier dysfunction, neutrophil and monocyte/ macrophage activation, adhesion molecule expression, initial factors, mast cell involvement and intracellular signaling in PALI. Different regulatory mechanisms exist in PALI and sepsis-induced lung injury. Endothelial barrier dysfunction occurs early on in acute pancreatitis and tumor necrosis factor (TNF)-a and monocyte chemoattractive protein-1 levels in the circulation gradually increase in acute pancreatitis. Leukocytes from the circulation, lung tissue and bronchoalveolar fluid exhibit different expression and activation patterns in the development of PALI. Mast cells seem to be involved in the initiation of leukocyte activation during the initial phase of PALI. Activation of the protein kinase C (PKC) signaling pathway could play an important role in the pathogenesis of PALI. Inhibition of PKC may be one candidate to prevent and treat the development of PALI.

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Alterations of Adhesion Molecule Expression and Inflammatory Mediators in Acute Lung Injury Induced by Septic and Non-septic Challenges

Cited by 16 publications

References 22 publications

Betulinic acid attenuates lung injury by modulation of inflammatory cytokine response in experimentally-induced polymicrobial sepsis in mice

Betulinic acid attenuates lung injury by modulation of inflammatory cytokine response in experimentally-induced polymicrobial sepsis in mice

Influence of dexamethasone on inflammatory mediators and NF-κB expression in multiple organs of rats with severe acute pancreatitis

A new understanding of pancreatitis-associated pulmonary injury

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