Effect of Immunoglobulin G on the Hepatic Microvascular Inflammatory Response During Sepsis

McCuskey, Robert S.; Nishida, Jiro; McDonnell, Deboragh; Baker, Gregory L.; Urbaschek, Renate; Urbaschek, B.

doi:10.1097/00024382-199601000-00007

Cited by 29 publications

(17 citation statements)

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“…The beneficial effect of the anti-E-selectin antibody was not caused by an unspecific IgG effect 48 because a number of studies showed that control IgG is not protective in this model. 19,26,27,32,34 In addition, IgG monoclonal antibodies against P-selectin, 19 platelet-endothelial cell adhesion molecule 1, 32 and L-selectin (Fig.…”

Section: Figmentioning

confidence: 82%

Pathophysiologic Importance of E– and L–Selectin for Neutrophil–Induced Liver Injury During Endotoxemia in Mice

et al. 2000

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Section: Figmentioning

confidence: 82%

Pathophysiologic Importance of E– and L–Selectin for Neutrophil–Induced Liver Injury During Endotoxemia in Mice

et al. 2000

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“…Because apoptosis in this model is entirely mediated by TNF-␣ (30,37), these findings suggest that Li et al may have reduced TNF levels with these antibodies. Although it remains unclear how this occurred, IgG has the capacity to bind ET and attenuate cytokine formation (42). Less TNF-␣ formation will result in reduced apoptosis, which is a critical event in neutrophil extravasation and injury (17,30,35).…”

Section: Discussionmentioning

confidence: 99%

Generation and functional significance of CXC chemokines for neutrophil-induced liver injury during endotoxemia

Dorman¹,

Gujral²,

Bajt³

et al. 2005

American Journal of Physiology-Gastrointestinal and Liver Physi

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The hypothesis that the neutrophil chemoattractant CXC chemokines KC and macrophage inflammatory protein-2 (MIP-2) are involved in neutrophil transmigration and liver injury was tested in C3Heb/FeJ mice treated with galactosamine (Gal, 700 mg/kg), endotoxin (ET, 100 microg/kg), or Gal + ET (Gal/ET). Hepatic KC and MIP-2 mRNA levels and plasma CXC chemokine concentrations were dramatically increased 1.5 h after Gal/ET or ET alone and gradually declined up to 7 h. Murine recombinant cytokines (TNF-alpha, IL-1 alpha, and IL-1 beta), but not Gal/ET, induced CXC chemokine formation in the ET-resistant C3H/HeJ strain. To assess the functional importance of KC and MIP-2, C3Heb/FeJ mice were treated with Gal/ET and control IgG or a combination of anti-KC and anti-MIP-2 antibodies. Anti-CXC chemokine antibodies did not attenuate hepatocellular apoptosis, sinusoidal neutrophil sequestration and extravasation, or liver injury at 7 h. Furthermore, there was no difference in liver injury between BALB/cJ wild-type and CXC receptor-2 gene knockout (CXCR2-/-) mice treated with Gal/ET. The higher neutrophil count in livers of CXCR2-/- than in wild-type mice after Gal/ET was caused by the elevated number of neutrophils located in sinusoids of untreated CXCR2-/- animals. The pancaspase inhibitor Z-Val-Ala-Asp-fluoromethylketone eliminated Gal/ET-induced apoptosis and neutrophil extravasation and injury but not CXC chemokine formation. Thus Gal/ET induced massive, cytokine-dependent CXC chemokine formation in the liver. However, neutrophil extravasation and injury occurred in response to apoptotic cell injury at 6-7 h and was independent of CXC chemokine formation.

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“…As apoptosis in this model is entirely TNF-dependent [7], the most likely explanation for reduced apoptosis is reduced TNF formation. In fact, injection of high doses of immunoglobulin G (IgG) has been shown to bind ET, which can reduce TNF formation by Kupffer cells [8]. The observation that all IgG treatment attenuated apoptosis and that the combination of two antibodies (twice the IgG dose) had an additive effect [1] is consistent with this explanation.…”

Section: Dear Editormentioning

confidence: 82%

Critical role of CXC chemokines in endotoxemic liver injury in mice

Jaeschke

Bajt

2004

Journal of Leukocyte Biology

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Effect of Immunoglobulin G on the Hepatic Microvascular Inflammatory Response During Sepsis

Cited by 29 publications

References 0 publications

Pathophysiologic Importance of E– and L–Selectin for Neutrophil–Induced Liver Injury During Endotoxemia in Mice

Pathophysiologic Importance of E– and L–Selectin for Neutrophil–Induced Liver Injury During Endotoxemia in Mice

Generation and functional significance of CXC chemokines for neutrophil-induced liver injury during endotoxemia

Critical role of CXC chemokines in endotoxemic liver injury in mice

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