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Muramyl dipeptide and toll-like receptor sensitivity in NOD2-associated Crohn's disease.

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Title: Muramyl dipeptide and toll-like receptor sensitivity in NOD2-associated Crohn's disease.
Authors: van Heel, David A., Ghosh, Subrata, Butler, Matt, Hunt, Karen A., Lundberg, Anna M. C., Ahmad, Tariq, McGovern, Dermot P. B., Onnie, Clive, Negoro, Kenichi, Goldthorpe, Sue, Foxwell, Brian M. J., Mathew, Christopher G., Forbes, Alastair, Jewell, Derek P., Playford, Raymond J.
Source: Lancet. 5/21/2005, Vol. 365 Issue 9473, p1794-1796. 3p. 2 Charts, 2 Graphs.
Subjects: Crohn's disease, Interleukin-8, Interleukins, Immune system, Medical research, Genetic research, Immunity
Abstract: Summary Both NOD2 (CARD15) alleles are mutated in roughly 15% of patients with Crohn's disease, but functional effects are unclear. We analyzed the cytokine response of peripheral blood mononuclear cells to muramyl dipeptide (MDP), the ligand for NOD2. MDP induced little TNFα or interleukin 1β, but strong interleukin-8 secretion. MDP also substantially upregulated secretion of TNFα and interleukin 1β induced by toll-like receptor ligands. These effects were abolished by the most common Crohn's NOD2 double mutant genotypes at low nanomolar MDP concentrations, and provide the basis to develop a test of NOD2 functional deficiency. In Crohn's disease, there are defects in neutrophil recruitment driven by NOD2 and interleukin 8 and in cross talk between the NOD2 and toll-like receptor pathways, which suggests that the immune system fails to receive an early priming signal. [ABSTRACT FROM AUTHOR]
Copyright of Lancet is the property of Lancet and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database: Psychology and Behavioral Sciences Collection
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  Data: Muramyl dipeptide and toll-like receptor sensitivity in NOD2-associated Crohn's disease.
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  Data: <searchLink fieldCode="AR" term="%22van+Heel%2C+David+A%2E%22">van Heel, David A.</searchLink><br /><searchLink fieldCode="AR" term="%22Ghosh%2C+Subrata%22">Ghosh, Subrata</searchLink><br /><searchLink fieldCode="AR" term="%22Butler%2C+Matt%22">Butler, Matt</searchLink><br /><searchLink fieldCode="AR" term="%22Hunt%2C+Karen+A%2E%22">Hunt, Karen A.</searchLink><br /><searchLink fieldCode="AR" term="%22Lundberg%2C+Anna+M%2E+C%2E%22">Lundberg, Anna M. C.</searchLink><br /><searchLink fieldCode="AR" term="%22Ahmad%2C+Tariq%22">Ahmad, Tariq</searchLink><br /><searchLink fieldCode="AR" term="%22McGovern%2C+Dermot+P%2E+B%2E%22">McGovern, Dermot P. B.</searchLink><br /><searchLink fieldCode="AR" term="%22Onnie%2C+Clive%22">Onnie, Clive</searchLink><br /><searchLink fieldCode="AR" term="%22Negoro%2C+Kenichi%22">Negoro, Kenichi</searchLink><br /><searchLink fieldCode="AR" term="%22Goldthorpe%2C+Sue%22">Goldthorpe, Sue</searchLink><br /><searchLink fieldCode="AR" term="%22Foxwell%2C+Brian+M%2E+J%2E%22">Foxwell, Brian M. J.</searchLink><br /><searchLink fieldCode="AR" term="%22Mathew%2C+Christopher+G%2E%22">Mathew, Christopher G.</searchLink><br /><searchLink fieldCode="AR" term="%22Forbes%2C+Alastair%22">Forbes, Alastair</searchLink><br /><searchLink fieldCode="AR" term="%22Jewell%2C+Derek+P%2E%22">Jewell, Derek P.</searchLink><br /><searchLink fieldCode="AR" term="%22Playford%2C+Raymond+J%2E%22">Playford, Raymond J.</searchLink>
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  Data: <searchLink fieldCode="JN" term="%22Lancet%22">Lancet</searchLink>. 5/21/2005, Vol. 365 Issue 9473, p1794-1796. 3p. 2 Charts, 2 Graphs.
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  Data: Summary Both NOD2 (CARD15) alleles are mutated in roughly 15% of patients with Crohn's disease, but functional effects are unclear. We analyzed the cytokine response of peripheral blood mononuclear cells to muramyl dipeptide (MDP), the ligand for NOD2. MDP induced little TNFα or interleukin 1β, but strong interleukin-8 secretion. MDP also substantially upregulated secretion of TNFα and interleukin 1β induced by toll-like receptor ligands. These effects were abolished by the most common Crohn's NOD2 double mutant genotypes at low nanomolar MDP concentrations, and provide the basis to develop a test of NOD2 functional deficiency. In Crohn's disease, there are defects in neutrophil recruitment driven by NOD2 and interleukin 8 and in cross talk between the NOD2 and toll-like receptor pathways, which suggests that the immune system fails to receive an early priming signal. [ABSTRACT FROM AUTHOR]
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  Data: <i>Copyright of Lancet is the property of Lancet and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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