Kupffer cell depletion partially prevents hepatic heme oxygenase 1 messenger RNA accumulation in systemic inflammation in mice: Role of interleukin 1β

Rizzardini, Milena; Zappone, Massimo; Villa, Pia; Gnocchi, Paola; Sironi, Marina; Diomede, Luisa; Meazza, Cristina; Monshouwer, Mario; Cantoni, L

doi:10.1002/hep.510270311

Cited by 57 publications

(44 citation statements)

References 50 publications

(52 reference statements)

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“…In our study, gadolinium administration does not seem to affect cytokine release in tissues outside the liver, since it did not modify serum concentrations of TNF-after LPS injection. Similar results have previously been observed by other authors (Kohno et al 1997, Rizzardini et al 1998, Kono et al 2001. Furthermore, Kono et al (2002) have reported that although gadolinium administration prevented LPS-induced increase in TNF-gene expression in the liver, it did not modify the serum concentrations of TNF-.…”

Section: Discussionsupporting

confidence: 89%

Inactivation of Kupffer cells by gadolinium administration prevents lipopolysaccharide-induced decrease in liver insulin-like growth factor-I and IGF-binding protein-3 gene expression

Granado¹,

Martín²,

Priego³

et al. 2006

Journal of Endocrinology

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Gram-negative bacterial infection or treatment of animals with bacterial lipopolysaccharide (LPS) induces a catabolic state with proteolysis, liver injury and an inhibition of the insulin-like growth factor-I (IGF-I) system. The purpose of this work was to elucidate the role of Kupffer cells in LPS-induced inhibition of the IGF-I/IGF-binding protein-3 (IGFBP-3) system. Adult male Wistar rats were either pretreated with the Kupffer cell inhibitor gadolinium chloride (10 mg/kg, i.v., 24 h prior to LPS exposure) or saline vehicle. Rats received two i.p. injections of 1 mg/kg LPS (at 17:30 and 08:30 h the following day) and were killed 4 h after the second injection. LPS administration induced a significant decrease in body weight and in serum concentrations of IGF-I and IGFBP-3 (P<0·01), as well as in their gene expression in the liver. LPS-injected rats had increased serum concentrations of ACTH, corticosterone (P<0·05), tumour necrosis factor-(TNF-) and nitrites (P<0·01). Pretreatment of the animals with gadolinium chloride blocked the inhibitory effect of LPS on body weight, and on serum concentrations of IGF-I, IGFBP-3 and nitrites, as well as growth hormone receptor (GHR), IGF-I and IGFBP-3 gene expression in the liver. In contrast, gadolinium chloride administration did not modify the stimulatory effect of LPS on serum concentrations of ACTH, corticosterone and TNF-. These results suggest that Kupffer cells are important mediators in the inhibitory effect of LPS on GHR, IGF-I and IGFBP-3 gene expression in the liver, leading to a decrease in serum concentrations of IGF-I and IGFBP-3.

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Section: Discussionsupporting

confidence: 89%

Inactivation of Kupffer cells by gadolinium administration prevents lipopolysaccharide-induced decrease in liver insulin-like growth factor-I and IGF-binding protein-3 gene expression

Granado¹,

Martín²,

Priego³

et al. 2006

Journal of Endocrinology

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“…Methyl palmitate (2 g/kg, i.v) was applied as an effective kupffer cells inhibitor and administered 44 hours before LPS. 30 Liver injury biomarkers were assessed 24 hours after antimalarial drugs administration in all experimental groups.…”

Section: Methodsmentioning

confidence: 99%

Concurrent Inflammation Augments Antimalarial Drugs-Induced Liver Injury in Rats

et al. 2016

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“…4 HO-1 expression is induced not only in response to its substrate heme, 8 but also by various stress stimuli such as hydrogen peroxide, xenobiotics, nitric oxide, ultraviolet-A radiation, heavy metals, hypoxia, hyperoxia, heat shock, 9,10 endotoxin 11,12 and proinflammatory cytokines. [13][14][15][16] Accumulating evidence reveals the protective role of HO-1 by virtue of the antiinflammatory, antiapoptotic and antiproliferative activities of the products released by the heme breakdown reaction. [17][18][19] The acute phase response (APR) is a defense reaction of the organism directed to restrict the area of damage and to eliminate, or at least isolate, the damaging agent.…”

mentioning

confidence: 99%

“…Although it has been shown that HO-1 could be upregulated under inflammatory conditions in the liver 15,16,22 and in hepatoma cell lines, 14 it remains unclear whether induction of HO-1 in vivo occurs as a response to cytokines released locally at the site of inflammation. To test this hypothesis, we analyzed HO-1 expression in the liver and extrahepatic tissues of rats after induction of sterile muscle abscess by injection of turpentine oil (TO), which subsequently leads to a local inflammation followed by systemic APR.…”

mentioning

confidence: 99%

Upregulation of heme oxygenase-1 gene by turpentine oil-induced localized inflammation: involvement of interleukin-6

Tron¹,

Novosyadlyy²,

Dudás³

et al. 2005

Laboratory Investigation

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Heme oxygenase-1 (HO-1) is the inducible isoform of an enzyme family responsible for heme degradation and was suggested to be involved in the acute phase response in the liver. However, the mechanisms of the HO-1 regulation under inflammatory conditions are poorly understood. Therefore, the purpose of the current work was to study the expression of HO-1 in the liver and other organs of rats with a localized inflammation after intramuscular injection of turpentine oil (TO). Since interleukin-6 (IL-6) is known to be a principal mediator of inflammation, the levels of this cytokine were also estimated in the animal model used. HO-1 and IL-6 expression was evaluated by Northern blot, in situ hybridization, Western blot, immunohistochemistry and enzyme-linked immunosorbent assay. In the liver and injured muscle, the HO-1 mRNA levels were dramatically increased 4-6 h after TO administration. HO-1 protein levels in the liver were elevated starting from 6-12 h after the treatment. In other internal organs such as the heart, kidney and large intestine, only a slight induction of HO-1 mRNA was observed. IL-6-specific transcripts appeared only in the injured muscle and were in accordance with serum levels of IL-6. In turn, temporal expression of IL-6 in the muscle and circulatory IL-6 levels correlated well with HO-1 expression in the liver and injured muscle. In the liver of control rats HO-1 protein was detected in Kupffer cells, while in TO-injected rats also hepatocytes became strongly HO-1 positive. Conversely, in the injured muscle, HO-1 immunoreactivity was attributed only to macrophages. Our data demonstrate that during localized inflammation HO-1 expression was rapidly and strongly induced in macrophages of injured muscle and in hepatocytes, and IL-6 derived from injured muscle seems to be responsible for the HO-1 induction in the liver.

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Kupffer cell depletion partially prevents hepatic heme oxygenase 1 messenger RNA accumulation in systemic inflammation in mice: Role of interleukin 1β

Cited by 57 publications

References 50 publications

Inactivation of Kupffer cells by gadolinium administration prevents lipopolysaccharide-induced decrease in liver insulin-like growth factor-I and IGF-binding protein-3 gene expression

Inactivation of Kupffer cells by gadolinium administration prevents lipopolysaccharide-induced decrease in liver insulin-like growth factor-I and IGF-binding protein-3 gene expression

Concurrent Inflammation Augments Antimalarial Drugs-Induced Liver Injury in Rats

Upregulation of heme oxygenase-1 gene by turpentine oil-induced localized inflammation: involvement of interleukin-6

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