Kupffer Cell Activation by Hydrogen Peroxide

Steib, Christian; Bilzer, Manfred; Härtl, Josef M.; Beitinger, Frigga; Gülberg, Veit; Göke, Burkhard; Gerbes, Alexander L.

doi:10.1097/shk.0b013e3181b85934

Cited by 13 publications

(9 citation statements)

References 21 publications

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“…The role of complement receptors binding C3a and C5a has also been established in Kupffer cell activation [12]. Recently, a new mechanism of Kupffer cell activation by hydrogen peroxide was proposed [24]. …”

Section: Pathophysiology Of Acute-on-chronic Liver Failurementioning

confidence: 99%

Bench-to-beside review: Acute-on-chronic liver failure - linking the gut, liver and systemic circulation

2011

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The concept of acute-on-chronic liver failure (ACLF) was introduced recently to describe a subset of patients with chronic liver disease presenting with profound deterioration of liver function and rapidly evolving multi-organ failure. ACLF is frequently accompanied by the development of severe inflammatory response syndrome and has a high mortality. To date, treatment options are limited and exclusively supportive. Over the last few years, some insights have been generated in the pathophysiology of ACLF. A key role for the interaction of innate immune dysfunction, enhanced bacterial translocation from the gut, and circulatory dysfunction has been proposed. In this respect, therapeutic strategies have been examined, with variable success, in experimental studies in animals and humans. This review focuses on potentially relevant pathophysiological elements in the development of ACLF and points out promising treatment modalities in ACLF.

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Section: Pathophysiology Of Acute-on-chronic Liver Failurementioning

confidence: 99%

Bench-to-beside review: Acute-on-chronic liver failure - linking the gut, liver and systemic circulation

2011

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“…The macrophages may be activated by the specific liver disease (e.g., virus, alcohol, steatosis, and drugs) where damage associated molecular patterns (DAMPs) activate macrophages accompanied by inflammation, fibrosis, and finally cirrhosis. Further, patients with liver cirrhosis and portal hypertension have intestinal edema and a leaky gut wall resulting in translocation of endotoxins and gut bacteria, e.g., pathogen associated molecular patterns (PAMPs), stimulating gastrointestinal and liver macrophages (Wiest and Garcia-Tsao, 2005;Wiest et al, 2014;Seitz et al, 2018) with secretion of inflammatory and vasoactive cytokines (Steib et al, 2007(Steib et al, , 2010a.…”

Section: Introductionmentioning

confidence: 99%

Divergences in Macrophage Activation Markers Soluble CD163 and Mannose Receptor in Patients With Non-cirrhotic and Cirrhotic Portal Hypertension

et al. 2021

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IntroductionMacrophages are involved in development and progression of chronic liver disease and portal hypertension. The macrophage activation markers soluble (s)CD163 and soluble mannose receptor (sMR), are associated with portal hypertension in patient with liver cirrhosis but never investigated in patients with non-cirrhotic portal hypertension. We hypothesized higher levels in cirrhotic patients with portal hypertension than patients with non-cirrhotic portal hypertension. We investigated sCD163 and sMR levels in patients with portal hypertension due to idiopathic portal hypertension (IPH) and portal vein thrombosis (PVT) in patients with and without cirrhosis.MethodsWe studied plasma sCD163 and sMR levels in patients with IPH (n = 26), non-cirrhotic PVT (n = 20), patients with cirrhosis without PVT (n = 31) and with PVT (n = 17), and healthy controls (n = 15).ResultsMedian sCD163 concentration was 1.51 (95% CI: 1.24–1.83) mg/L in healthy controls, 1.96 (95% CI: 1.49–2.56) in patients with non-cirrhotic PVT and 2.16 (95% CI: 1.75–2.66) in patients with IPH. There was no difference between non-cirrhotic PVT patients and healthy controls, whereas IPH patients had significantly higher levels than controls (P < 0.05). The median sCD163 was significantly higher in the cirrhotic groups compared to the other groups, with a median sCD163 of 6.31 (95% CI: 5.16–7.73) in cirrhotics without PVT and 5.19 (95% CI: 4.18–6.46) with PVT (P < 0.01, all). Similar differences were observed for sMR.ConclusionSoluble CD163 and sMR levels are elevated in patients with IPH and patients with cirrhosis, but normal in patients with non-cirrhotic PVT. This suggests that hepatic macrophage activation is more driven by the underlying liver disease with cirrhosis than portal hypertension.

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“…; Friedman, 2008a,b; Steib et al, 2010), cellular activation by apoptotic bodies (Zernecke et al, 2009), and release of cellular debris from necrotic cells (Jaeschke et al, 2002). Chemokines function as paracrine signals and in autocrine loops, with both positive and negative feedback elements.…”

Section: Introductionmentioning

confidence: 99%

The Role of Chemokines in Acute Liver Injury

Saiman¹,

Friedman²

2012

Front. Physio.

153

130

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Chemokines are small molecular weight proteins primarily known to drive migration of immune cell populations. In both acute and chronic liver injury, hepatic chemokine expression is induced resulting in inflammatory cell infiltration, angiogenesis, and cell activation and survival. During acute injury, massive parenchymal cell death due to apoptosis and/or necrosis leads to chemokine production by hepatocytes, cholangiocytes, Kupffer cells, hepatic stellate cells, and sinusoidal endothelial cells. The specific chemokine profile expressed during injury is dependent on both the type and course of injury. Hepatotoxicity by acetaminophen for example leads to cellular necrosis and activation of Toll-like receptors while the inciting insult in ischemia reperfusion injury produces reactive oxygen species and subsequent production of pro-inflammatory chemokines. Chemokine expression by these cells generates a chemoattractant gradient promoting infiltration by monocytes/macrophages, NK cells, NKT cells, neutrophils, B cells, and T cells whose activity are highly regulated by the specific chemokine profiles within the liver. Additionally, resident hepatic cells express chemokine receptors both in the normal and injured liver. While the role of these receptors in normal liver has not been well described, during injury, receptor up-regulation, and chemokine engagement leads to cellular survival, proliferation, apoptosis, fibrogenesis, and expression of additional chemokines and growth factors. Hepatic-derived chemokines can therefore function in both paracrine and autocrine fashions further expanding their role in liver disease. More recently it has been appreciated that chemokines can have diverging effects depending on their temporal expression pattern and the type of injury. A better understanding of chemokine/chemokine receptor axes will therefore pave the way for development of novel targeted therapies for the treatment of liver disease.

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Kupffer Cell Activation by Hydrogen Peroxide

Cited by 13 publications

References 21 publications

Bench-to-beside review: Acute-on-chronic liver failure - linking the gut, liver and systemic circulation

Bench-to-beside review: Acute-on-chronic liver failure - linking the gut, liver and systemic circulation

Divergences in Macrophage Activation Markers Soluble CD163 and Mannose Receptor in Patients With Non-cirrhotic and Cirrhotic Portal Hypertension

The Role of Chemokines in Acute Liver Injury

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