Is glucosamine safe in patients with seafood allergy?

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• 作者：Heather C. Gray ; Patricia S. Hutcheson ; Raymond G. Slavin
• 关键词：Bronchial epithelial cells ; ERK1/2 ; GM-CSF ; MAP kinase ; Raf1
• 刊名：Journal of Allergy and Clinical Immunology
• 出版年：2004
• 出版时间：August 2004
• 年：2004
• 卷：114
• 期：2
• 页码：459-460
• 全文大小：55 K

文摘

ML-1 (IL-17F) is a recently discovered cytokine, and its function remains elusive. GM-CSF is a crucial cytokine for the maturation of various cell types and regulates allergic airway inflammation.me=""toc2""><h3 class=""h3"">Objectiveh3>

The functional effect of ML-1 in the expression of GM-CSF was investigated.me=""toc3""><h3 class=""h3"">Methodsh3>

The levels of gene and protein expression in normal human bronchial epithelial cells (NHBEs) in the presence or absence of various kinase inhibitors or, in some cases, of a Raf1 dominant-negative mutant were determined by RT-PCR and ELISA, respectively. Western blotting was performed to investigate kinase activation.me=""toc4""><h3 class=""h3"">Resultsh3>

The results showed first that ML-1 induces, in a time-dependent and dose-dependent manner, the gene and protein expression for GM-CSF NHBEs, which are associated with activation of Raf1 and MAP kinase kinase (MEK) kinases. Selective MEK inhibitors, PD98059 and U0126, and Raf1 kinase inhibitor I significantly inhibited ML-1–induced GM-CSF production. Furthermore, overexpression of Raf1 dominant-negative mutants inhibited IL-17F–induced GMCSF expression. The combination of PD98059 and Raf1 kinase inhibitor I completely blocked GM-CSF production, whereas 2 protein kinase C inhibitors, Ro-31-7549 and GF109203X, and a phosphatidylinositol 3-kinase inhibitor, LY294002, showed no inhibitory effect.me=""toc5""><h3 class=""h3"">Conclusionh3>

These findings suggest that ML-1 induces GM-CSF expression through the activation of the Raf1-MEK–extracellular signal-regulated kinase 1/2 pathway.