Author(s): Mitić Katarina, Miletić Tatjana, Kovačević-Jovanović Vesna, Kuštrimović Nataša, Kosec D, Dimitrijević Mirjana, Stanojević Stanislava
Keywords:experimental autoimmune encephalomyelitis (EAE), hydrogen peroxide (H2O2), nitric oxide (NO), phagocytosis, peritoneal cells phenotype, rat strains
We have investigated the phenotype of peritoneal cells and the functions of peritoneal macrophages obtained from experimental autoimmune encephalomyelitis (EAE)-susceptible Dark Agouti (DA) and EAE-resistant Albino Oxford (AO) rat strains on days 1, 3 and 7 post immunization with encephalitogen. Resident peritoneal cells from immunized and non-immunized rats of both strains were subjected to flow cytometric analyses and after adherence were tested for zymosan phagocytosis, hydrogen peroxide (H2O2) and nitric oxide (NO) production. In non-immunized rats, macrophages from the DA rat strain phagocytosed more zymosan but produced less H2O2 than cells from the AO strain, while both strains produced comparable amounts of NO. Immunization increased phagocytosis in DA rats' cells, but decreased both phagocytosis and H2O2 production in cells from AO rats. Overall higher phagocyte ability in DA rats was associated with a significantly larger population of ED1+ cells (macrophages and dendritic cells), in contrast to a more pronounced expression of ED2 antigen (resident macrophages) on cells from AO rats. Immunization also increased the expression of CD11b molecule on non-resident ED2– macrophages of DA, but not of AO rats. The early and subtle phenotype changes in peritoneal cells of both rat strains might mirror the mechanism contributing to their different sensitivity to the induction of autoimmunity.
Indexing: Thomson Reuters/Science Citation Index Expanded, Zoological Record, Biosis Previews, Web of Science, Journal Citation Reports, Google Scholar, SCIndeks, KoBSON, Genamics, Journal Seek, Research Gate, DOAJ, Journal Rate, SJR – SCImago Journal & Country Rank, WorldCat, Academic Journals Database, Medical Journals Links, MedSci, Pubget