Pregled bibliografske jedinice broj: 418283
Ingestion of apoptotic cells by bone marrow macrophages and modulation of antiinflammatory response
Ingestion of apoptotic cells by bone marrow macrophages and modulation of antiinflammatory response // 2008 Annual Meeting of the Croatian Immunological Society / Rabatić S. i sur. (ur.).
Zagreb: Hrvatsko imunološko društvo, 2008. (predavanje, domaća recenzija, sažetak, znanstveni)
CROSBI ID: 418283 Za ispravke kontaktirajte CROSBI podršku putem web obrasca
Naslov
Ingestion of apoptotic cells by bone marrow macrophages and modulation of antiinflammatory response
Autori
Kozmar, Ana ; Bohlson S., Suzanne
Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, znanstveni
Izvornik
2008 Annual Meeting of the Croatian Immunological Society
/ Rabatić S. i sur. - Zagreb : Hrvatsko imunološko društvo, 2008
Skup
2008 Annual Meeting of the Croatian Immunological Society
Mjesto i datum
Šibenik, Hrvatska, 09.10.2008. - 12.10.2008
Vrsta sudjelovanja
Predavanje
Vrsta recenzije
Domaća recenzija
Ključne riječi
apoptosis; bone marrow macrophages; inflammatory response
Sažetak
Rapid ingestion of apoptotic cells in the absence of inflammation is required for maintenance of normal tissue homeostasis. Recognition of apoptotic cells by phagocytes is complex, involving numerous receptor-ligand interactions. Previous studies have attributed much of this activity to the presence of phosphatidylserine (PS) on the plasma membrane of apoptotic cells. Here we demonstrate a system where the pro-phagocytic and anti-inflammatory properties of apoptotic cells have been separated and are independent of PS. Cell lines Jurkat and Hela were rendered apoptotic with etoposide and actinomycin-D, respectively. Accessibility of PS was confirmed cytofluorometrically by staining with FITC-conjugated annexin V on both cell lines. As expected, apoptotic Jurkat and Hela cells were preferentially ingested by bone marrow macrophages over live or necrotic Jurkats and Hela cells. Detection of PS on the outer membrane of apoptotic Jurkat and Hela cells was similar. Coculture of apoptotic Hela cells with Raw264.7 cells stably expressing an NFκ B or TNFα luciferase reporter gene resulted in an inhibition of luciferase activity and in attenuation of TNFα secretion in response to LPS treatment. This inhibition in proinflammatory activity was also demonstrated using primary bone marrow macrophages that failed to produce TNFα in response to LPS treatment when cultured in the presence of apoptotic Hela cells. Interestingly, Jurkat cells that were rendered apoptotic with etoposide were unable to alter the proinflammatory cytokine production in response to LPS in Raw264.7 cells stably expressing luciferase driven by the NFκ B or TNFα reporter. Here we provide a system to delineate signals required for macrophage engulfment of apoptotic cells independent of signals leading to alteration of proinflammatory cytokine production which should be useful in identifying the critical molecular components required in both of these processes.
Izvorni jezik
Engleski
Znanstvena područja
Kliničke medicinske znanosti
POVEZANOST RADA
Projekti:
214-1081874-0168 - Regulacijski limfociti u sistemskim autoimunim bolestima (Malenica, Branko, MZOS ) ( CroRIS)
Ustanove:
Klinički bolnički centar Zagreb
Profili:
Ana Kozmar
(autor)