Influence of Apoptotic Bodies and Apoptotic Microvesicles on NO Production in Macrophages
- Autores: Schwartz Y.1, Dolganova O.2, Rudina M.1, Pyshnaya I.3, Bgatova N.4
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Afiliações:
- Novosibirsk Research Institute of Tuberculosis, Ministry of Health of the Russian Federation
- Novosibirsk State Medical University, Ministry of Health of the Russian Federation
- Institute of Chemical Biology and Fundamental Medicine, Siberian Division of the Russian Academy of Sciences
- Research Institute of Clinical and Experimental Lymphology, Affiliated Branch of Federal Research Centre Institute of Cytology and Genetics, Siberian Division of the Russian Academy of Sciences
- Edição: Volume 165, Nº 4 (2018)
- Páginas: 453-456
- Seção: Article
- URL: https://journals.rcsi.science/0007-4888/article/view/240410
- DOI: https://doi.org/10.1007/s10517-018-4192-9
- ID: 240410
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Resumo
We studied the effect of extracellular vesicular particles generated during apoptosis by macrophages of M0, M1 and M2 phenotypes on spontaneous and LPS-stimulated production of NO. The fractions of apoptotic bodies and apoptotic microvesicles were obtained in the primary cultures of peritoneal macrophages undergoing apoptosis. The effect of these microparticles on LPS-induced proinflammatory response of recipient macrophages critically depends on the initial phenotype of “donor” macrophages. Microvesicles and especially apoptotic bodies from M1 macrophages stimulate basal NO production. LPS stimulation of these macrophages preincubated with apoptotic bodies was not followed by further growth of NO production; in macrophages preincubated with microvesicles, LPS even suppressed NO production. Apoptotic microparticles obtained from M2 macrophages produced little effect on the basal production of NO. LPS stimulation of macrophages-recipients preincubated with microparticles from M2 macrophages did not enhance NO production. Incubation of macrophages with apoptotic microparticles induces the formation of endotoxic tolerance.
Sobre autores
Ya. Schwartz
Novosibirsk Research Institute of Tuberculosis, Ministry of Health of the Russian Federation
Autor responsável pela correspondência
Email: YShSchwartz@mail.ru
Rússia, Novosibirsk
O. Dolganova
Novosibirsk State Medical University, Ministry of Health of the Russian Federation
Email: YShSchwartz@mail.ru
Rússia, Novosibirsk
M. Rudina
Novosibirsk Research Institute of Tuberculosis, Ministry of Health of the Russian Federation
Email: YShSchwartz@mail.ru
Rússia, Novosibirsk
I. Pyshnaya
Institute of Chemical Biology and Fundamental Medicine, Siberian Division of the Russian Academy of Sciences
Email: YShSchwartz@mail.ru
Rússia, Novosibirsk
N. Bgatova
Research Institute of Clinical and Experimental Lymphology, Affiliated Branch of Federal Research Centre Institute of Cytology and Genetics, Siberian Division of the Russian Academy of Sciences
Email: YShSchwartz@mail.ru
Rússia, Novosibirsk
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