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12 results on '"Breese, Emma J"'

5. Relationship between endogenous colony stimulating factors and apoptosis in human colon cancer cells: role of cyclo-oxygenase inhibitors

Author

Calatayud, Sara, Warner, Timothy D, Breese, Emma J, and Mitchell, Jane A

Subjects
Dose-Response Relationship, Drug, Tumor Necrosis Factor-alpha, Macrophage Colony-Stimulating Factor, Anti-Inflammatory Agents, Non-Steroidal, Granulocyte-Macrophage Colony-Stimulating Factor, Apoptosis, Colony-Stimulating Factors, Papers, Colonic Neoplasms, Granulocyte Colony-Stimulating Factor, Humans, Cyclooxygenase Inhibitors, HT29 Cells, Interleukin-1
Abstract

1. Nonsteroidal anti-inflammatory drug (NSAID) usage is associated with gastrointestinal inflammatory damage and aggravation of gut inflammatory conditions. NSAIDs also exert a preventive effect against colon cancer that seems to be due to increased colon cell apoptosis. NSAIDs have been shown to modulate the release of colony stimulating factors (CSFs) in some cells. In the present study we analysed the effect of these drugs on secretion of CSFs and apoptosis in human colon epithelial cells (HT-29). 2. HT-29 cells secreted bioactive levels of GM-CSF, G-CSF and M-CSF when stimulated with IL-1ss and TNF-alpha, and diclofenac (10(-7)-10(-4) M), indomethacin (10(-7)-10(-4) M) and sodium salicylate (10(-5)-10(-2) M) induced concentration-dependent increases in GM-CSF secretion. 3. Reduced secretion of G-CSF and M-CSF and increased cell apoptosis were observed with the highest concentrations of these non-selective NSAIDs. 4. No changes in any CSF release or HT-29 cell apoptosis were detected in the presence of the COX-2 selective inhibitor DFP (10(-7)-10(-4) M). 5. Neither the exogenous addition of CSFs nor the blockade of secreted CSFs modified apoptosis in HT-29 cells stimulated with cytokines and/or NSAIDs. 6. These results suggest that colon epithelial cells can contribute to local inflammatory responses by releasing CSFs and thus extend the life span of local leukocytes. Modulation of CSF levels by non-selective NSAIDs may be involved in the pro-inflammatory effects of these agents in the gut.

Published
2001

12. The Frequency of Cells Secreting Interferon-? and Interleukin-4, -5, and -10 in the Blood and Duodenal Mucosa of Children with Cow's Milk Hypersensitivity

Author

Hauer, A Christina, Breese, Emma J, Walker-Smith, John A, and MacDonald, Thomas T

Abstract

Enzyme-linked immunoabsorbant spots (ELISPOTs) have been used to analyze the frequency of cells spontaneously secreting interferon-? (INF-?), IL-4, IL-5, or IL-10 in mononuclear cells isolated from the blood of children with cow's milk-sensitive enteropathy (CMSE), cow's milk allergy (CMA), and age-matched controls. In addition, cytokine profiles of duodenal lamina propria lymphocytes were compared in patients with CMSE and control subjects. In blood, spontaneous cytokine-secreting cells were uncommon, but there was significantly increased IFN-?, IL-4, IL-5, and IL-10 ELISPOTs in children with CMSE and CMA compared with control subjects. IL-4 ELISPOTs were significantly greater in the blood of children with CMA compared with those with CMSE. In the lamina propria the frequencies of spontaneous cytokine-secreting cells were high compared with that in blood. Significantly increased ELISPOTs for IFN-? and IL-4 were found in CMSE compared with controls. IL-5 ELISPOTs were unchanged, and IL-10 ELISPOTs were reduced in CMSE compared with controls. These results show a general enhancement of Th1and Th2-type cytokine-secreting cells in the blood of children with cow's milk hypersensitivity, although the increased IL-4-secreting cells in blood in CMA may be of relevance in view of the fact that this disease is IgE-mediated. In the lamina propria, there is also enhancement of IFN-?- and IL-4-secreting cells in CMSE compared with control subjects; however, cells secreting IFN-? are 10 times more numerous than cells secreting IL-4, showing a dominance of Th1-type responses in both controls and CMSE patients.

Published
1997
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