The Response of Liver Macrophages to Inflammatory Stimulation.

Decker, Karl

doi:10.2302/kjm.47.1

Cited by 53 publications

(34 citation statements)

References 26 publications

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“…LYZ was used in this study as a marker to demonstrate the KCs number and shape in the liver for LYZ is a reliable and stable marker for mononuclearphagocyte system, which only exists in the KCs in the liver. The change of KCs shape and LYZ content in KCs illustrate the change of KCs function [11] . Activated KCs appeared round in shape with increasing LYZ content in the cytoplasm.…”

Section: Immunohistochemical Staining Of Lyz-positive Cells In Rat Livermentioning

confidence: 87%

Dynamic changes and mechanism of intestinal endotoxemia in partially hepatectomized rats

Liu²,

Liu³

et al. 2007

WJG

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AIM:To explore the mechanism of intestinal endotoxemia (IETM) formation and its changes in partially hepatectomized (PH) rats. METHODS:One-hundred and two adult male Wistar rats were randomly divided into three groups: normal control (NC) group, partially hepatectomized (PH) group and a sham-operated (SO) group. To study the dynamic changes, rats were sacrificed before and at different time points after partial hepatectomy or the sham-operation ( 6 h, 12 h, 24 h, 36 h, 48 h, 72 h, 120 h and 168 h). NC group was used as 0h time point in observation, namely 0 h group. For each time point indicated, six rats were used in parallel. Endotoxin (ET) and diamine oxidase (DAO) levels were determined in serum using Limulus Lysate test with chromogenic substrate and spectrophotometry. Intestinal mucosa barrier was observed under optical or electron microscope. The number and functional state of Kupffer cells (KCs) in the remnant regenerating liver were measured by immunohistochemical staining. RESULTS:Serum ET levels significantly increased during 6-72 h period after PH compared with NC and SO groups, and there were two peak values at 12 and 48 h while serum DAO level significantly increased at 12 and 24 h. There was positive correlation (r = 0.757, P < 0.05) between the levels of DAO and ET dynamic changes. The optical examination showed neutrophil margination and superficial necrosis of the villi in the intestinal mucosa during 6-24 h period after PH. The penetrated electron microscope examination showed that the gaps between intestinal mucosa cells were increased and the Lanthanum (La) particles were observed among the intestinal mucosa cells during 6-48 h period. The numbers of KCs in the remnant regenerating liver were significantly increased during 24-168 h period after PH. However, the activation of KCs was predominantly observed at 48 h after PH. CONCLUSION:The mechanism of IETM in PH rats might be the injury of intestinal mucosa barrier and the decrease of the absolute number of KCs as well as the depression of functional state of KCs. This observation is of potential value in patients undergoing liver resection.

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Section: Immunohistochemical Staining Of Lyz-positive Cells In Rat Livermentioning

confidence: 87%

Dynamic changes and mechanism of intestinal endotoxemia in partially hepatectomized rats

Liu²,

Liu³

et al. 2007

WJG

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“…The Kupffer cells were selected for detailed analysis because they are known to play a central role in the host hepatic response to various inflammatory triggers. 21,22 Antibodies to F4/80 identified Kupffer cells within sinusoidal vessels in sections derived from tumor or saline-injected mice. Staining for TNF-␣ in control, saline-injected mice was either negative or low ( Figure 1A).…”

Section: Increased Kupffer Cell-associated Tnf-␣ Production In Responmentioning

confidence: 99%

Characterization of the Host Proinflammatory Response to Tumor Cells during the Initial Stages of Liver Metastasis

Khatib

Auguste

Fallavollita

et al. 2005

The American Journal of Pathology

132

120

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The liver is a major site of metastases for some of the most common human malignancies, carcinomas of the gastrointestinal tract in particular. Liver metastases are frequently inoperable and are associated with poor prognosis. 1 The metastatic cascade involves a sequence of steps that can lead to tumor cell arrest in the vascular bed of an invaded organ such as the liver and subsequently to tumor extravasation into the extravascular space.2 These events are regulated by, and in turn, can induce host proinflammatory responses that involve tumor-and host-derived chemokines and cytokines. A key mediator of the inflammatory response is tumor necrosis factor (TNF)-␣. This cytokine can play a dual role in tumor progression and metastasis. On one hand it can inhibit tumor growth through its cytocidal and proapoptotic activities but on the other, it can promote tumor progression through different mechanisms such as the induction of vascular endothelial adhesion receptors and the promotion of growth, invasion, and metastasis. The ultimate effect of TNF-␣ may depend on its concentrations, on tumor cell susceptibility, and on the stage of the disease. 3,4

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“…Inflammatory mediators, like cytokines, nitric oxide (NO), reactive oxygen species (ROS) and eicosanoids are released during infection and inflammation by activated macrophages from various sources, including liver and lung (8,9,15). The release of these mediators is intended as defence against invading pathogens, however excessive release can be detrimental to the host and aggravate disease leading to e.g.…”

Section: Introductionmentioning

confidence: 99%

Suppression of the acute inflammatory response of porcine alveolar‐ and liver macrophages

Izeboud¹,

Monshouwer

Witkamp

et al. 2000

Veterinary Quarterly

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During infection and inflammation drug disposition and hepatic metabolism are markedly affected in mammals. Pro-inflammatory mediators play an important role in the suppression of (cytochrome-P450-mediated) drug metabolism. Inflammatory mediators like cytokines, nitric oxide (NO), reactive oxygen species (ROS) and eicosanoids are released by activated macrophages from various sources, including liver and lung. It was the aim of this study to investigate ways to suppress the activation of macrophages during the onset of the inflammatory cascade. Therefore porcine lung and liver macrophages were isolated, and incubated with lipopolysaccharide (LPS) to initiate an acute inflammatory response, represented by the release of high amounts of tumour necrosis factor-a (TNF-a) into the culture medium. Additionally the primary macrophages were coincubated with phosphodiesterase-IV-(PDE-IV)-inhibitors or B-adrenoceptor agonists that in previous studies demonstrated strong suppressive effects on TNF-a release. Especially the B-adrenoceptor agonists showed to be very potent TNF-a suppressants, which indicates that the B-adrenoceptor might be an interesting target for suppression of activation of macrophages. This was strengthened by the observation that the B-adrenoceptor expression was not altered during the onset of the inflammatory cascade.

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The Response of Liver Macrophages to Inflammatory Stimulation.

Cited by 53 publications

References 26 publications

Dynamic changes and mechanism of intestinal endotoxemia in partially hepatectomized rats

Dynamic changes and mechanism of intestinal endotoxemia in partially hepatectomized rats

Characterization of the Host Proinflammatory Response to Tumor Cells during the Initial Stages of Liver Metastasis

Suppression of the acute inflammatory response of porcine alveolar‐ and liver macrophages

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