Modulation of lipopolysaccharide-induced production of cytokines by methionine-enkephalin
Autor: | Tihomir Balog, Sabina Rabatić, Ivo Hršak, Tatjana Marotti, Blanka Burek |
---|---|
Rok vydání: | 1994 |
Předmět: |
Lipopolysaccharides
Male medicine.medical_specialty Erythrocytes Lipopolysaccharide Phagocytosis medicine.medical_treatment Enkephalin Methionine Immunology Neuropeptide Biology Tumour necrosis factor Interleukin-1 Methionine-enkephalin chemistry.chemical_compound Mice Internal medicine medicine Immunology and Allergy Macrophage Animals Tumor Necrosis Factor-alpha Interleukin Endocrinology Cytokine chemistry Cell culture Macrophages Peritoneal Mice Inbred CBA Tumor necrosis factor alpha |
Zdroj: | Immunology letters. 40(1) |
ISSN: | 0165-2478 |
Popis: | In the present study, we have examined the effect of opioid peptide methionine enkephalin (MENK) on production of factors with interleukin-1 (IL-1) and tumor necrosis factor (TNF) activity by mouse peritoneal macrophages and assessed whether modification in the production of those cytokines could be related to alteration of phagocytosis by MENK. None of the MENK concentrations examined altered IL-1 or TNF activity alone. However, peritoneal macrophages co-stimulated with 1 microgram of lipopolysaccharide (LPS) and 10(-10) M MENK potentiated IL-1 activity, compared to LPS alone, but abrogated TNF activity induced by LPS. While MENK alone slightly decreased phagocytosis of sheep red blood cells (SRBC) by mouse peritoneal macrophages, cells simultaneously incubated with 1 microgram of LPS and 10(-10) M MENK had increased phagocytosis compared to LPS alone. Moreover, phagocytosis of SRBC by cells incubated overnight with the supernatant of the respective cell culture was significantly augmented. These results provide additional evidence for the immunoregulatory role of neuropeptides and suggest that the modulatory action of MENK could be mediated, at least in part, through the up-regulation of cytokines, most probably IL-1 and TNF. |
Databáze: | OpenAIRE |
Externí odkaz: |