The effects of Gamijinhae-tang on elastase/lipopolysaccharide-induced lung inflammation in an animal model of acute lung injury

Sohn, Sung-Hwa; Jang, HaRyeon; Kim, Youngeun; Jang, Young Pyo; Cho, Seung-Hun; Jung, Hee-Jae; Jung, Sung Il; Bae, Hyunsu

doi:10.1186/1472-6882-13-176

Cited by 12 publications

(17 citation statements)

References 68 publications

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“…Endotoxin, the bacterial LPS, is considered an important factor in the development of ALI, which increases the pulmonary endothelial paracellular and transcellular permeability that causes pulmonary oedema [ 3 ]. LPS has been widely adopted for in vivo and in vitro studies of endothelial permeability injury mode [ 26 - 28 ]. In this study, we used an EC permeability injury model induced by LPS, which caused an increase in EC paracellular permeability in a time- and dose-dependent manner.…”

Section: Discussionmentioning

confidence: 99%

Interaction between mesenchymal stem cells and endothelial cells restores endothelial permeability via paracrine hepatocyte growth factor in vitro

et al. 2015

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IntroductionMesenchymal stem cells (MSCs) have potent stabilising effects on vascular endothelium injury, inhibiting endothelial permeability in lung injury via paracrine hepatocyte growth factor (HGF). Recently, it has been indicated that MSCs secrete more factors by MSC-endothelial cell (MSC-EC) interactions. We hypothesised that MSC-EC interactions restore endothelial permeability induced by lipopolysaccharide (LPS) via paracrine HGF.MethodsWe investigated the endothelial permeability induced by LPS under two co-culture conditions. Human pulmonary microvascular endothelial cells (HPMECs) were added into the upper chambers of cell-culture inserts, while two different co-culture conditions were used in the lower side of the transwells, as follows: (1) MSC-EC interaction group: MSCs and HPMECs contact co-culture; (2) MSC group: MSCs only. The endothelial paracellular and transcellular permeabilities in the upper side of transwells were detected. Then the concentration of HGF was measured in the culture medium by using an enzyme-linked immunosorbent assay kit, followed by neutralisation of HGF with anti-HGF antibody in the co-culture medium. In addition, adherens junction and cytoskeleton protein expressions were measured by Western blot and immunofluorescence. HPMEC proliferation was analysed by bromodeoxyuridine incorporation assay.ResultsThe paracellular permeability significantly increased after LPS stimulation in a dose-dependent and time-dependent manner. Meanwhile, MSC-EC interaction more significantly decreased endothelial paracellular and transcellular permeability induced by LPS. Moreover, HGF levels in the MSC-EC interaction group were much higher than those of the MSC group. However, neutralising HGF with anti-HGF antibody inhibited the role of MSC-EC interaction in improving endothelial permeability. Compared with the MSC group, MSC-EC interaction increased vascular endothelial (VE)-cadherin and occludin protein expression, reduced caveolin-1 protein expression in HPMECs, and restored remodelling of F-actin and junctional localisation of VE-cadherin. Furthermore, the proliferation ratio in the MSC-EC interaction group was higher than that of the MSC group. However, the effects of MSCs were significantly blocked by anti-HGF antibody.ConclusionsThese data suggested that MSC-EC interaction decreased endothelial permeability induced by LPS, which was attributed mainly to HGF secreted by MSCs. The main mechanisms by which HGF restored the integrity of endothelial monolayers were remodelling of endothelial intercellular junctions, decreasing caveolin-1 protein expression, and inducing proliferation in HPMECs.Electronic supplementary materialThe online version of this article (doi:10.1186/s13287-015-0025-1) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Interaction between mesenchymal stem cells and endothelial cells restores endothelial permeability via paracrine hepatocyte growth factor in vitro

et al. 2015

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“…A single LPS exposure induces pulmonary inflammation in many animals, characterized by neutrophil and macrophage influx [200][201][202][203][204][205]. Chronic exposure to LPS induces structural changes to the murine and guinea pig lung, which persist after LPS exposure has ceased, mediated primarily by increases in TNF-α, IFN-γ, and IL-18 [203,[206][207][208][209][210]. The advantages of using LPS-induced inflammation and fibrosis models over other models such as CS include the relatively short time frame to achieve pathological features of COPD [211].…”

Section: Lipopolysaccharide Exposurementioning

confidence: 99%

Animal Models Reflecting Chronic Obstructive Pulmonary Disease and Related Respiratory Disorders: Translating Pre-Clinical Data into Clinical Relevance

Tanner

Single

2019

J Innate Immun

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Chronic obstructive pulmonary disease (COPD) affects the lives of an ever-growing number of people worldwide. The lack of understanding surrounding the pathophysiology of the disease and its progression has led to COPD becoming the third leading cause of death worldwide. COPD is incurable, with current treatments only addressing associated symptoms and sometimes slowing its progression, thus highlighting the need to develop novel treatments. However, this has been limited by the lack of experimental standardization within the respiratory disease research area. A lack of coherent animal models that accurately represent all aspects of COPD clinical presentation makes the translation of promising in vitro data to human clinical trials exceptionally challenging. Here, we review current knowledge within the COPD research field, with a focus on current COPD animal models. Moreover, we include a set of advantages and disadvantages for the selection of pre-clinical models for the identification of novel COPD treatments.

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“…For example, mice could be intranasally challenged with PPE and LPS for 4 weeks to induce COPD - like lung inflammation [77]. In another study, increased inflammatory response was observed following rats exposure to a combination of LPS and CS.…”

Section: Combination Inducersmentioning

confidence: 99%

“…Also, in a mouse model of PPE and LPS-induced COPD, airway remodeling, lung inflammation, goblet cell hyperplasia, and alveolar enlargement were observed [77]. Similarly, emphysematous destruction, parenchymal inflammation, mucus hyper secretion and airway remodeling in a mouse model of COPD, were reported after CS exposure [29, 30, 32, 64, 118, 119].…”

Section: Measured Parametersmentioning

confidence: 99%

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Experimental animal models for COPD: a methodological review

Ghorani¹,

Boskabady²,

Khazdair³

et al. 2017

Tob. Induced Dis.

164

111

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IntroductionChronic obstructive pulmonary disease (COPD) is a progressive disorder that makes the breathing difficult and is characterized by pathological conditions ranging from chronic inflammation to tissue proteolysis. With regard to ethical issues related to the studies on patients with COPD, the use of animal models of COPD is inevitable. Animal models improve our knowledge about the basic mechanisms underlying COPD physiology, pathophysiology and treatment. Although these models are only able to mimic some of the features of the disease, they are valuable for further investigation of mechanisms involved in human COPD.MethodsWe searched the literature available in Google Scholar, PubMed and ScienceDirect databases for English articles published until November 2015. For this purpose, we used 5 keywords for COPD, 3 for animal models, 4 for exposure methods, 3 for pathophysiological changes and 3 for biomarkers. One hundred and fifty-one studies were considered eligible for inclusion in this review.ResultsAccording to the reviewed articles, animal models of COPD are mainly induced in mice, guinea pigs and rats. In most of the studies, this model was induced by exposure to cigarette smoke (CS), intra-tracheal lipopolysaccharide (LPS) and intranasal elastase. There were variations in time course and dose of inducers used in different studies. The main measured parameters were lung pathological data and lung inflammation (both inflammatory cells and inflammatory mediators) in most of the studies and tracheal responsiveness (TR) in only few studies.ConclusionThe present review provides various methods used for induction of animal models of COPD, different animals used (mainly mice, guinea pigs and rats) and measured parameters. The information provided in this review is valuable for choosing appropriate animal, method of induction and selecting parameters to be measured in studies concerning COPD.

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The effects of Gamijinhae-tang on elastase/lipopolysaccharide-induced lung inflammation in an animal model of acute lung injury

Cited by 12 publications

References 68 publications

Interaction between mesenchymal stem cells and endothelial cells restores endothelial permeability via paracrine hepatocyte growth factor in vitro

Interaction between mesenchymal stem cells and endothelial cells restores endothelial permeability via paracrine hepatocyte growth factor in vitro

Animal Models Reflecting Chronic Obstructive Pulmonary Disease and Related Respiratory Disorders: Translating Pre-Clinical Data into Clinical Relevance

Experimental animal models for COPD: a methodological review

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