Hepatoprotective role of interleukin 10 in galactosamine/lipopolysaccharide mouse liver injury

Louis, Hubert; Moine, Olivier Le; Peny, Marie-Odile; Gulbis, Béatrice; Nisol, F; Goldman, Michel; Devière, Jacques

doi:10.1053/gast.1997.v112.pm9041256

Cited by 113 publications

(87 citation statements)

References 3 publications

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“…Differential efficacy of IL-10 neutralization in these mouse strains was probably due to different serum levels of TNF-␣. IL-10 has been found to limit TNF-␣ secretion after low dose LPS challenge (47). Yet serum levels of both TNF-␣ and IL-10 were higher in LFA-1 Ϫ/Ϫ mice than in heterozygous littermates.…”

Section: Discussionmentioning

confidence: 98%

“…IL-10 plays a protective role in low dose LPS-induced shock/ liver injury (46,47). After low dose LPS challenge, serum levels of IL-10 were significantly, although modestly, higher in LFA-1 Ϫ/Ϫ mice than in LFA-1 ϩ/Ϫ and C57BL/6 mice.…”

Section: Discussionmentioning

confidence: 99%

“…Elevated serum levels of IL-10 in LFA-1 Ϫ/Ϫ mice following low dose LPS challenge IL-10 plays a protective role against both high dose (43-45) and low dose LPS-induced shock (46,47). To determine whether IL-10 participates in the increased resistance of LFA-1 Ϫ/Ϫ mice to low dose LPS-induced shock, serum levels of IL-10 were compared in LFA-1 Ϫ/Ϫ , LFA-1 ϩ/Ϫ , and C57BL/6 mice following challenge with LPS and D-GalN.…”

Section: Markedly Reduced Numbers Of Platelets In the Liver Of Lfa-1 mentioning

confidence: 99%

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Increased Resistance of LFA-1-Deficient Mice to Lipopolysaccharide-Induced Shock/Liver Injury in the Presence of TNF-α and IL-12 Is Mediated by IL-10: A Novel Role for LFA-1 in the Regulation of the Proinflammatory and Anti-Inflammatory Cytokine Balance

Emoto¹,

Emoto²,

Brinkmann

et al. 2003

The Journal of Immunology

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Challenge with low doses of LPS together with d-galactosamine causes severe liver injury, resulting in lethal shock (low dose LPS-induced shock). We examined the role of LFA-1 in low dose LPS-induced shock. LFA-1−/− mice were more resistant to low dose LPS-induced shock/liver injury than their heterozygous littermates, although serum levels of TNF-α and IL-12 were higher in these mice. C57BL/6 mice were not rescued from lethal effects of LPS by depletion of NK1+ cells, granulocytes, or macrophages, and susceptibility of NKT cell-deficient mice was comparable to that of controls. High numbers of platelets were detected in the liver of LFA-1+/− mice after low dose LPS challenge, whereas liver accumulation of platelets was only marginal in LFA-1−/− mice. Following low dose LPS challenge, serum levels of IL-10 were higher in LFA-1−/− mice than in LFA-1+/− mice, and susceptibility to low dose LPS-induced shock as well as platelet accumulation in the liver of LFA-1−/− mice were markedly increased by IL-10 neutralization. Serum levels of IL-10 in LFA-1+/− mice were only marginally affected by macrophage depletion. However, in LFA-1−/− mice macrophage depletion markedly reduced serum levels of IL-10, and as a corollary, susceptibility of LFA-1−/− mice to low dose LPS-induced shock was markedly elevated despite the fact that TNF-α levels were also diminished. We conclude that LFA-1 participates in LPS-induced lethal shock/liver injury by regulating IL-10 secretion from macrophages and that IL-10 plays a decisive role in resistance to shock/liver injury. Our data point to a novel role of LFA-1 in control of the proinflammatory/anti-inflammatory cytokine network.

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Section: Markedly Reduced Numbers Of Platelets In the Liver Of Lfa-1 mentioning

confidence: 99%

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Increased Resistance of LFA-1-Deficient Mice to Lipopolysaccharide-Induced Shock/Liver Injury in the Presence of TNF-α and IL-12 Is Mediated by IL-10: A Novel Role for LFA-1 in the Regulation of the Proinflammatory and Anti-Inflammatory Cytokine Balance

Emoto¹,

Emoto²,

Brinkmann

et al. 2003

The Journal of Immunology

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show abstract

“…This dose was previously demonstrated to inhibit liver Kupffer cells in rats and mice. [20][21][22] The purpose of this experiment was to determine if inhibition of the liver Kupffer cells would change the binding of the 99m TcAd5K in the liver. Mice were killed after 1 h, biodistribution determined, and results were compared with 99m TcAd5K without GdCl 3 pretreatment (Table 2).…”

Section: Dose-dependent Liver Accumulation Of 99m Tc-ad5kmentioning

confidence: 99%

Imaging and tissue biodistribution of 99mTc-labeled adenovirus knob (serotype 5)

Zinn

Smyth

et al. 1998

Gene Ther

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“…The elucidation of factors that promote hepatic regeneration after acute injury has garnered considerable attention and the list of hepatic regenerative factors now includes numerous endogenously generated growth factors such as hepatocyte growth factor and basic fibroblast growth factor and immunomodulatory cytokines, such as interleukin-10. 11,12 In addition, hepatic regeneration following acute injury due to experimental ischemia/reperfusion, hepatectomy or hepatotoxin exposure also appears to require the regulated involvement of proinflammatory mediators such as interleukin1alpha (IL-1␣), tumor necrosis factor-alpha (TNF-␣) and interleukin-6. [13][14][15][16] More recently, ELR-containing CXC chemokines have emerged as important cytokine parti-cipants in models of liver injury.…”

Section: Introductionmentioning

confidence: 99%

Macrophage inflammatory protein-2 gene therapy attenuates adenovirus- and acetaminophen-mediated hepatic injury

et al. 1999

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Hepatoprotective role of interleukin 10 in galactosamine/lipopolysaccharide mouse liver injury

Cited by 113 publications

References 3 publications

Increased Resistance of LFA-1-Deficient Mice to Lipopolysaccharide-Induced Shock/Liver Injury in the Presence of TNF-α and IL-12 Is Mediated by IL-10: A Novel Role for LFA-1 in the Regulation of the Proinflammatory and Anti-Inflammatory Cytokine Balance

Increased Resistance of LFA-1-Deficient Mice to Lipopolysaccharide-Induced Shock/Liver Injury in the Presence of TNF-α and IL-12 Is Mediated by IL-10: A Novel Role for LFA-1 in the Regulation of the Proinflammatory and Anti-Inflammatory Cytokine Balance

Imaging and tissue biodistribution of 99mTc-labeled adenovirus knob (serotype 5)

Macrophage inflammatory protein-2 gene therapy attenuates adenovirus- and acetaminophen-mediated hepatic injury

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