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- 저자 : Seoane, Silvia (검색결과 3 건)
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In vitro response of rat microglia and human polymorphonuclear cells (PMN) to immunoactive compounds
Lombardi, Valter RM,Eetcheverria, Ignacio,Fernandez-Novoa, Lucia,Diaz, Joaquin,Seoane, Silvia,Cacabelos, Ramon Kyung Hee Oriental Medicine Research Center 2005 Oriental pharmacy and experimental medicine Vol.5 No.3
Although the field of study in immune enhancing compounds is relatively new, natural products from plants represent a rich and promising source of novel molecules with immunomodulating properties, Microglial cells, the main immune effector cells of the brain, usually display a ramified morphology and low expression levels of immunologically relevant antigens such as MHC class I and class II. Since any compound which participates in activation of phagocytic cells contributes to the production of potentially toxic factors, the search for convenient in vitro test-systems and study of mechanisms of action of these agents are of great interest. Human blood polymorphonuclear (PMN) cells and primary microglial cells isolated from Sprague-Dawley rats were used as cellular screening tests for study of phagocytosis-stimulating action of immunomodulating agents. Numbers of phagocytic activity were evaluated by the phagocyte ingestion of yeast cells and NO-synthase activity, nitrite production, and nitroblue tetrazolium test were determined after phagocyte stimulation. It was possible to demonstrate that indexes of phagocytic activity can be used as quantitative indicators for measurement immunomodulating activity. As a positive control, Zymosan A-induced phagocytosis in both PMN cells and primary microglial cells was used. $IFN-{\gamma}$ (0.1 -1 U/ml) stimulated phagocytosis in PMN cells 1.2 times after 2 - 3 h incubation, although at higher concentrations (10 - 100 U/ml) it strongly inhibited phagocytosis. In a similar way, at higher concentrations, $IFN-{\gamma}$ (100 - 500 U/ml) suppressed phagocytosis in zymosan-A stimulated microglial cells. When Polypodium leucotomus, cambricum and vulgare extracts were tested alone, increased levels of phagocytosis were observed in PMN. In addition, microglial cells showed both increased phagocytosis and MHC class-II antigen expressions. Surprisingly, when PMN and microglia were treated with a combination of Polypodium and $IFN-{\gamma}$, phagocytosis was not inhibited. We did not find changes in NO-synthase activity and nitrite production in both microglia and PMN cells activated by different immunomodulating agents. These results indicate that primary microglial cell cultures as well as human PMN cells can provide reproducible quantitative results in screening phagocytic activity of different immunoactive compounds. Furthermore, both inhibitory or activation mechanisms might be studied using these in vitro experimental approaches.
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Comparative Molecular Analysis of Gastrointestinal Adenocarcinomas
Liu, Yang,Sethi, Nilay S.,Hinoue, Toshinori,Schneider, Barbara G.,Cherniack, Andrew D.,Sanchez-Vega, Francisco,Seoane, Jose A.,Farshidfar, Farshad,Bowlby, Reanne,Islam, Mirazul,Kim, Jaegil,Chatila, Wa Elsevier 2018 Cancer cell Vol.33 No.4
<P><B>Summary</B></P> <P>We analyzed 921 adenocarcinomas of the esophagus, stomach, colon, and rectum to examine shared and distinguishing molecular characteristics of gastrointestinal tract adenocarcinomas (GIACs). Hypermutated tumors were distinct regardless of cancer type and comprised those enriched for insertions/deletions, representing microsatellite instability cases with epigenetic silencing of <I>MLH1</I> in the context of CpG island methylator phenotype, plus tumors with elevated single-nucleotide variants associated with mutations in <I>POLE</I>. Tumors with chromosomal instability were diverse, with gastroesophageal adenocarcinomas harboring fragmented genomes associated with genomic doubling and distinct mutational signatures. We identified a group of tumors in the colon and rectum lacking hypermutation and aneuploidy termed genome stable and enriched in DNA hypermethylation and mutations in <I>KRAS</I>, <I>SOX9</I>, and <I>PCBP1</I>.</P> <P><B>Highlights</B></P> <P> <UL> <LI> GI adenocarcinomas comprised five molecular subtypes: EBV, MSI, HM-SNV, CIN, and GS </LI> <LI> Hypermutated tumors had diverse immune features varying by tissue and subtype </LI> <LI> CIN tumors displayed more fragmented copy-number alterations in the upper GI tract </LI> <LI> Genome-stable CRC subtype was enriched for recurrent mutations in <I>SOX9</I> and <I>PCBP1</I> </LI> </UL> </P> <P><B>Graphical Abstract</B></P> <P>[DISPLAY OMISSION]</P>
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