Neutrophil migration in inflammation: nitric oxide inhibits rolling, adhesion and induces apoptosis
| Autor: | Sandra Oliveira, João Santana da Silva, Fernando Q. Cunha, Daniela Dal Secco, Juliane Alves Paron, Sergio H. Ferreira |
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| Rok vydání: | 2003 |
| Předmět: |
Lipopolysaccharides
Male Cancer Research Endothelium Neutrophils Physiology Clinical Biochemistry Nitric Oxide Synthase Type II Apoptosis Leukocyte Rolling Inflammation Pharmacology Carrageenan Nitric Oxide Guanidines Nitroarginine Biochemistry Nitric oxide Mice chemistry.chemical_compound Cell Adhesion medicine Animals Enzyme Inhibitors Rats Wistar Cell adhesion Mice Knockout biology Chemistry Chemotaxis Rats N-Formylmethionine Leucyl-Phenylalanine Nitric oxide synthase Chemotaxis Leukocyte medicine.anatomical_structure Immunology biology.protein Nitric Oxide Synthase medicine.symptom |
| Zdroj: | Nitric Oxide. 9:153-164 |
| ISSN: | 1089-8603 |
| DOI: | 10.1016/j.niox.2003.11.001 |
| Popis: | There is controversy in the literature over whether nitric oxide (NO) released during the inflammatory process has a pro- or inhibitory effect on neutrophil migration. The aim of the present investigation was to clarify this situation. Treatment of rats with non-selective, NG-nitro-L-arginine (nitro), or selective inducible NO synthase (iNOS), aminoguanidine (amino) inhibitors enhanced neutrophil migration 6h after the administration of low, but not high, doses of carrageenan (Cg) or Escherichia coli endotoxin (LPS). The neutrophil migration induced by N-formyl-methionyl-leucyl-phenylalanine (fMLP) was also enhanced by nitro or amino treatments. The enhancement of Cg-induced neutrophil migration by NOS inhibitor treatments was reversed by co-treatment with L-arginine, suggesting an involvement of the L-arginine/NOS pathway in the process. The administration of Cg in iNOS deficient (iNOS(-/-)) mice also enhanced the neutrophil migration compared with wild type mice. This enhancement was markedly potentiated by treatment of iNOS(-/-) mice with nitro. Investigating the mechanisms by which NOS inhibitors enhanced the neutrophil migration, it was observed that they promoted an increase in Cg-induced rolling and adhesion of leukocytes to endothelium and blocked the apoptosis of emigrated neutrophils. Similar results were observed in iNOS(-/-) mice, in which these mechanisms were potentiated and reverted by nitro and L-arginine treatments, respectively. In conclusion, these results suggest that during inflammation, NO released by either constitutive NOS (cNOS) or iNOS down-modulates the neutrophil migration. This NO effect seems to be a consequence of decreased rolling and adhesion of the neutrophils on endothelium and also the induction of apoptosis in migrated neutrophils. |
| Databáze: | OpenAIRE |
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