The role of nitric oxide in parasitic diseases
| Autor: | Liew Fy |
|---|---|
| Rok vydání: | 1993 |
| Předmět: |
Necrosis
Lipopolysaccharide medicine.medical_treatment 030231 tropical medicine Down-Regulation Nitric Oxide Nitric oxide Interferon-gamma Mice 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Interferon 030225 pediatrics Parasitic Diseases medicine Animals Humans Macrophage Protein kinase A biology Macrophages Rats Cell biology Nitric oxide synthase Infectious Diseases Cytokine chemistry Enzyme Induction Immunology biology.protein Cytokines Parasitology Amino Acid Oxidoreductases Nitric Oxide Synthase medicine.symptom medicine.drug |
| Zdroj: | Annals of Tropical Medicine & Parasitology. 87:637-642 |
| ISSN: | 1364-8594 0003-4983 |
| Popis: | Murine macrophages express high levels of nitric oxide synthase and produce large amounts of nitric oxide (NO) when stimulated with certain cytokines in the presence of a trace amount of lipopolysaccharide (LPS). The stimulatory cytokines include interleukin-1 (IL-1), interferon-gamma (IFN-gamma), tumour necrosis factor-alpha (TNF-alpha) and migration inhibitory factor. Activated macrophages are highly effective killers of intra- and extra-cellular pathogens. However, as excessive NO can lead to immunopathology (diabetes, graft-v.-host disease, EAE, liver cirrhosis, rheumatoid arthritis), NO production is necessarily under tight regulation. A number of cytokines, including IL-4, IL-10 and transforming growth factor-beta, can down regulate the induction of NO synthase in macrophages. In addition, macrophages exposed to LPS alone and then stimulated with a mix of IFN-gamma and LPS express significantly lower levels of NO synthase than cells stimulated without pre-exposure to LPS. Furthermore, NO can reduce the activity of NO synthase by feedback inhibition, and also inhibit the production of IFN-gamma by Th1 cells (thus turning off its own synthesis from upstream). The regulatory pathways involve tyrosine kinase and protein kinase C. |
| Databáze: | OpenAIRE |
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