Sa1162 Transcriptional Profiling of Peripheral Blood Mononuclear Cells Identifies Genes and Gene Pathways Associated With Pediatric IBD and That Differentiate Crohn's Disease and Ulcerative Colitis

2014 ◽  
Vol 146 (5) ◽  
pp. S-216
Author(s):  
Jess L. Kaplan ◽  
Manoj Bhasin ◽  
Christopher J. Moran ◽  
Towia A. Libermann ◽  
Harland Winter
Keyword(s):  
Ulcerative Colitis ◽  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Peripheral Blood Mononuclear Cells ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Transcriptional Profiling ◽  
Peripheral Blood Mononuclear ◽  
Blood Mononuclear Cells ◽  
Pediatric Ibd

scholarly journals Lipopolysaccharide and silica-stimulated mononuclear cell prostaglandin production in ulcerative colitis

2000 ◽  
Vol 9 (3-4) ◽  
pp. 189-191
Author(s):  
Neville A. Punchard ◽  
John Cason ◽  
Jonathan Mullins ◽  
Chaman Chander ◽  
Richard P. H. Thompson
Keyword(s):  
Ulcerative Colitis ◽  
Crohn’S Disease ◽  
Mononuclear Cell ◽  
Peripheral Blood Mononuclear Cells ◽  
Peripheral Blood ◽  
Healthy Subjects ◽  
Mononuclear Cells ◽  
Peripheral Blood Mononuclear ◽  
Prostaglandin Production ◽  
Blood Mononuclear Cells

Basal, lipopolysaccharide (LPS) and silica-stimulated prostaglandin (PG) production were compared between peripheral blood mononuclear cells (PBMNC) from UC patients and healthy subjects (HS). Basal and LPS-stimulated PBMNC PGI2, but not PGE2, production was greater in UC. LPS stimulated both PGE2and PGI2by PBMNC from HS and UC patients. Silica stimulated production of both PGs by cells from HS but only PGE2by cells from UC patients. The differences in responses to silica and LPS may result from differences in activation of NFκB or, alternatively, prior sensitisation to one of these agents. That PBMNC PGE2production is not increased in UC, as it is in Crohn’s disease, suggests that there are differences in PBMNC behaviour between these two diseases.

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