Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1999-7-20
pubmed:abstractText
Tissue accumulation of polymorphonuclear neutrophils (PMN) in Inflammatory Bowel disease (IBD) might be, in part, due to a delay in apoptotic processes associated with the effects of their specific growth factors and inflammatory cytokines. We addressed this hypothesis by examining the activity of granulocyte colony-stimulating factor (G-CSF) and granulocyte-macrophage CSF (GM-CSF) in the organ culture supernatants of colonic mucosal specimens and their regulatory effects on PMN apoptosis in patients with IBD. The contents of G-CSF and GM-CSF in the supernatants were measured by the enzyme-linked immunosorbent assays and PMN apoptosis was evaluated by acridine orange/ethidium bromide staining, respectively. Mucosal specimens obtained from patients with active IBD exhibited higher levels of G-CSF and GM-CSF activity than controls. Notably, the levels of G-CSF activity were approximately 1000-fold higher than those of GM-CSF activity. Freshly isolated PMN showed a time-related increase in the proportion of cells with characteristic features of apoptosis when they were incubated with the culture medium alone and exposure of PMN to recombinant G-CSF and GM-CSF caused a concentration-dependent inhibition of apoptosis. Incubation of PMN with the supernatants from patients with active IBD induced an inhibitory effect on PMN apoptosis; this effect was abrogated to a significant degree by pre-incubation of the supernatants with anti-G-CSF serum. This study suggests that PMN apoptosis may be delayed under the influence of soluble mediators, especially G-CSF, in the microenvironment of IBD-affected mucosa, thus providing possible mechanisms for tissue accumulation of PMN in IBD.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0815-9319
pubmed:author
pubmed:issnType
Print
pubmed:volume
14
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
46-53
pubmed:dateRevised
2009-11-3
pubmed:meshHeading
pubmed-meshheading:10029277-Acridine Orange, pubmed-meshheading:10029277-Adolescent, pubmed-meshheading:10029277-Adult, pubmed-meshheading:10029277-Aged, pubmed-meshheading:10029277-Aged, 80 and over, pubmed-meshheading:10029277-Apoptosis, pubmed-meshheading:10029277-Culture Media, Conditioned, pubmed-meshheading:10029277-Culture Techniques, pubmed-meshheading:10029277-Cytokines, pubmed-meshheading:10029277-Ethidium, pubmed-meshheading:10029277-Female, pubmed-meshheading:10029277-Granulocyte Colony-Stimulating Factor, pubmed-meshheading:10029277-Granulocyte-Macrophage Colony-Stimulating Factor, pubmed-meshheading:10029277-Humans, pubmed-meshheading:10029277-Inflammatory Bowel Diseases, pubmed-meshheading:10029277-Intestinal Mucosa, pubmed-meshheading:10029277-Male, pubmed-meshheading:10029277-Middle Aged, pubmed-meshheading:10029277-Neutrophils
pubmed:year
1999
pubmed:articleTitle
Increased mucosal production of granulocyte colony-stimulating factor is related to a delay in neutrophil apoptosis in Inflammatory Bowel disease.
pubmed:affiliation
First Department of Internal Medicine, Nagoya University School of Medicine, Japan.
pubmed:publicationType
Journal Article, In Vitro