Dynamic changes of tissue factor pathway inhibitor type 2 associated with IL-1β and TNF-α in the development of murine acute lung injury

Li, Zhengwu; Mao, Zuohua; Lin, Yiqin; Wang, Liang; Jiang, Fanglin; Tang, Qiqun; Ma, Ding

doi:10.1016/j.thromres.2008.03.019

Cited by 7 publications

(6 citation statements)

References 28 publications

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“…At the protein level, TNF-α expression peaked within 4 h after LPS challenge and slowly declined over 24 h (Bozinovski et al, 2004). A comparable 24-h TNF-α expression pattern was reported in mice exposed to intravenous LPS (Li et al, 2008). Finally, neutrophil infiltration into the lungs was evident within 2 h after transnasal LPS challenge in mice (Bozinovski et al, 2004).…”

Section: Differential Regulation Of Lipopolysaccharide-related Signalsupporting

confidence: 66%

“…Similarly, MyD88 protein levels were elevated at 24 h after intraperitoneal LPS challenge although remaining at a plateau level over 2-3 days (Oshikawa and Sugiyama, 2003). In complete contrast, MAPK and TNF-α showed a more transient expression pattern after intravenous LPS reaching peak levels within the first few hours and returning to basal levels within 12-24 h (Li et al, 2008;Liu et al, 2008). These experimental findings indicate that the pathophysiological pathways of LPS are time-dependent and imply that signaling molecules are differentially activated during disease progression.…”

Section: Dynamics Of Lipopolysaccharide-induced Lung Injurymentioning

confidence: 94%

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Molecular Dynamics of Lipopolysaccharide-Induced Lung Injury in Rodents

et al. 2020

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Acute respiratory distress syndrome (ARDS) is a common disease entity in critical care medicine and is still associated with a high mortality. Because of the heterogeneous character of ARDS, animal models are an insturment to study pathology in relatively standardized conditions. Rodent models can bridge the gap from in vitro investigations to large animal and clinical trials by facilitating large sample sizes under physiological conditions at comparatively low costs. One of the most commonly used rodent models of acute lung inflammation and ARDS is administration of lipopolysaccharide (LPS), either into the airways (direct, pulmonary insult) or systemically (indirect, extra-pulmonary insult). This narrative review discusses the dynamics of important pathophysiological pathways contributing to the physiological response to LPS-induced injury. Pathophysiological pathways of LPS-induced lung injury are not only influenced by the type of the primary insult (e.g., pulmonary or extra-pulmonary) and presence of additional stimuli (e.g., mechanical ventilation), but also by time. As such, findings in animal models of LPS-induced lung injury may depend on the time point at which samples are obtained and physiological data are captured. This review summarizes the current evidence and highlights uncertainties on the molecular dynamics of LPS-induced lung injury in rodent models, encouraging researchers to take accurate timing of LPS-induced injury into account when designing experimental trials.

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Section: Differential Regulation Of Lipopolysaccharide-related Signalsupporting

confidence: 66%

Section: Dynamics Of Lipopolysaccharide-induced Lung Injurymentioning

confidence: 94%

Molecular Dynamics of Lipopolysaccharide-Induced Lung Injury in Rodents

et al. 2020

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“…Thus, in vitro , stimulation of human endothelial cells with inflammatory mediators such as LPS, and TNF-α significantly increases TFPI-2 expression [45]. Analogously, in vivo in a murine model, TFPI-2 expression is dramatically upregulated in the liver and in the lungs during LPS stimulation [46], [47]. These data, together with previous findings on release of C-terminal fragments by neutrophil elastase and their presence in human wounds [32], and as shown herein, particularly in association with bacteria ( Figure 2D ), suggest that TFPI-2 fragments may exert physiological roles during infection.…”

Section: Discussionmentioning

confidence: 99%

The TFPI-2 Derived Peptide EDC34 Improves Outcome of Gram-Negative Sepsis

et al. 2013

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Sepsis is characterized by a dysregulated host-pathogen response, leading to high cytokine levels, excessive coagulation and failure to eradicate invasive bacteria. Novel therapeutic strategies that address crucial pathogenetic steps during infection are urgently needed. Here, we describe novel bioactive roles and therapeutic anti-infective potential of the peptide EDC34, derived from the C-terminus of tissue factor pathway inhibitor-2 (TFPI-2). This peptide exerted direct bactericidal effects and boosted activation of the classical complement pathway including formation of antimicrobial C3a, but inhibited bacteria-induced activation of the contact system. Correspondingly, in mouse models of severe Escherichia coli and Pseudomonas aeruginosa infection, treatment with EDC34 reduced bacterial levels and lung damage. In combination with the antibiotic ceftazidime, the peptide significantly prolonged survival and reduced mortality in mice. The peptide's boosting effect on bacterial clearance paired with its inhibiting effect on excessive coagulation makes it a promising therapeutic candidate for invasive Gram-negative infections.

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“…MIP‐1α, the member of the CC chemokines, is secreted by activated T cells, B cells, monocytes, and mast cells and can induce chemotaxis of various types of leukocytes (Murdoch and Finn,2000; Mackay,2001). It has been reported that MIP‐1α is abundantly expressed in BAL fluid, which is closely associated with the development of fibrosis (Li et al,2008). Previous report had observed high expression of both IL‐1β and MIP‐1α in lungs of LPS‐induced ALI mice (Jeyaseelan et al,2004), which is consistent with our result.…”

Section: Discussionmentioning

confidence: 99%

Protective Effect of Resveratrol on Acute Lung Injury Induced by Lipopolysaccharide in Mice

Cao

Jing

Tang

et al. 2011

The Anatomical Record

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Resveratrol, a phytoalexin found in a range of plant products, may exert a variety of pharmacological activities. In this study, we investigated the effect of resveratrol on acute lung injury (ALI) induced by lipopolysaccharide (LPS) in vivo, and we found that the pretreatment with resveratrol can effectively protect mice against LPS-induced ALI. Mice were pretreated with 1 mg/kg resveratrol for 3 days before challenging with a dose of 15 mg/ kg LPS. The histological result showed that resveratrol can suppress the edema, inflammatory cell infiltration, and alveolar structure damage of lungs in ALI mice, and a decrease in the lung W/D ratio was also observed in mice with resveratrol pretreatment. Additionally, resveratrol markedly decreased the production of inflammatory cytokines, including IL-1b and MIP-1a and prevented the release of nitric oxide (NO) through inhibiting the expression of inducible NO synthase in lung tissues. Furthermore, the pretreatment with resveratrol suppressed the nuclear translocation of NFjB in lung tissues, which may be partly responsible for its effect on the ALI. In conclusion, the results presented here may suggest resveratrol as a potential therapeutic agent for treating ALI in the future. Anat Rec, 294:527-532, 2011. V V C 2011 Wiley-Liss, Inc.Key words: resveratrol; acute lung injury; lipopolysaccharide; NF-jB Acute lung injury (ALI) is a common clinical problem, which is characterized by the upregulation of inflammatory mediators in the host and followed by an onset of dyspnea, severe hypoxemia, and pulmonary edema, thus leading to significant morbidity and mortality (Erickson et al., 2009;Martinez et al., 2009). Several animal models have been developed to study the pathophysiologic mechanism involved in ALI, and the intraperitoneal injection of lipopolysaccharide (LPS), a component of the outer cell wall of most gram-negative bacteria, is one of the most common accepted models. ALI represents a state of excess production of inflammatory mediators, including cytokines, chemokines, and adhesion molecules (Ware and Matthay, 2000); and the release of LPS is a major stimulus for release of cytokines, which may further cause pulmonary damage leading to ALI (Ware et al., 2007). Although great advances in understanding the pathophysiology of ALI had been achieved, the available therapies have not reduced the mortality or increased the quality of life in survivors.Upregulation of inducible nitric oxide synthase (iNOS) increased the production of nitric oxide (NO), which was observed in ALI both in animal models and humans

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Dynamic changes of tissue factor pathway inhibitor type 2 associated with IL-1β and TNF-α in the development of murine acute lung injury

Cited by 7 publications

References 28 publications

Molecular Dynamics of Lipopolysaccharide-Induced Lung Injury in Rodents

Molecular Dynamics of Lipopolysaccharide-Induced Lung Injury in Rodents

The TFPI-2 Derived Peptide EDC34 Improves Outcome of Gram-Negative Sepsis

Protective Effect of Resveratrol on Acute Lung Injury Induced by Lipopolysaccharide in Mice

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