The effect of an interleukin receptor antagonist (IL-1ra) on colonocyte eicosanoid release
We investigated whether an interleukin 1 receptor antagonist (IL-1ra) altered cellular release of prostanoids and leukotrienes in a transformed colonic cell line (CACO-2) in the presence of proinflammatory stimuli. Cellular inflammation was induced by treatment with lipopolysaccharide (LPS) or the c...
| Auteurs principaux: | , , , , , , |
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| Format: | Article |
| Langue: | English |
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Hindawi Limited
1996-01-01
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| Collection: | Mediators of Inflammation |
| Accès en ligne: | http://dx.doi.org/10.1155/S0962935196000622 |
| _version_ | 1827083520472776704 |
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| author | G. S. Smith C. Rieckenberg W. E. Longo D. L. Kaminski J. E. Mazuski Y. Deshpande T. A. Miller |
| author_facet | G. S. Smith C. Rieckenberg W. E. Longo D. L. Kaminski J. E. Mazuski Y. Deshpande T. A. Miller |
| author_sort | G. S. Smith |
| collection | DOAJ |
| description | We investigated whether an interleukin 1 receptor antagonist (IL-1ra) altered cellular release of prostanoids and leukotrienes in a transformed colonic cell line (CACO-2) in the presence of proinflammatory stimuli. Cellular inflammation was induced by treatment with lipopolysaccharide (LPS) or the cytokine, interleukin 1 beta (IL-1β). In a separate set of experiments, cells were pretreated with IL-1ra prior to exposure to LPS or IL-1β. Prostaglandin E2 and leukotriene B4 (LTB4) levels were quantified by ELISA assays. Both LPS and IL-1β exposure were noted to stimulate cellular PGE2 release, a response which was significantly inhibited by IL-1ra treatment. Either stimulant when administered alone failed to stimulate release of LTB4. When administered after IL-1ra pretreatment however, both stimuli caused a significant increase in LTB4 release. These results suggest that a cytokine receptor antagonist can selectively influence eicosanoid production in this cell line. Furthermore, this study suggests that a IL-1ra may have a future clinical role in the treatment of inflammatory disorders of the colon which are intimately linked to enhanced eicosanoid synthesis. |
| first_indexed | 2025-03-20T03:50:27Z |
| format | Article |
| id | doaj.art-a56a835f6d204b789ab8d9f41c743a7b |
| institution | Directory Open Access Journal |
| issn | 0962-9351 1466-1861 |
| language | English |
| last_indexed | 2025-03-20T03:50:27Z |
| publishDate | 1996-01-01 |
| publisher | Hindawi Limited |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj.art-a56a835f6d204b789ab8d9f41c743a7b2024-10-03T05:57:54ZengHindawi LimitedMediators of Inflammation0962-93511466-18611996-01-015644945210.1155/S0962935196000622The effect of an interleukin receptor antagonist (IL-1ra) on colonocyte eicosanoid releaseG. S. Smith0C. Rieckenberg1W. E. Longo2D. L. Kaminski3J. E. Mazuski4Y. Deshpande5T. A. Miller6Department of Surgery, Saint Louis University School of Medicine, Health Sciences Center, 3635 Vista Avenue at Grand Boulevard, St Louis 63110-0250, Missouri, USADepartment of Surgery, Saint Louis University School of Medicine, Health Sciences Center, 3635 Vista Avenue at Grand Boulevard, St Louis 63110-0250, Missouri, USADepartment of Surgery, Saint Louis University School of Medicine, Health Sciences Center, 3635 Vista Avenue at Grand Boulevard, St Louis 63110-0250, Missouri, USADepartment of Surgery, Saint Louis University School of Medicine, Health Sciences Center, 3635 Vista Avenue at Grand Boulevard, St Louis 63110-0250, Missouri, USADepartment of Surgery, Saint Louis University School of Medicine, Health Sciences Center, 3635 Vista Avenue at Grand Boulevard, St Louis 63110-0250, Missouri, USADepartment of Surgery, Saint Louis University School of Medicine, Health Sciences Center, 3635 Vista Avenue at Grand Boulevard, St Louis 63110-0250, Missouri, USADepartment of Surgery, Saint Louis University School of Medicine, Health Sciences Center, 3635 Vista Avenue at Grand Boulevard, St Louis 63110-0250, Missouri, USAWe investigated whether an interleukin 1 receptor antagonist (IL-1ra) altered cellular release of prostanoids and leukotrienes in a transformed colonic cell line (CACO-2) in the presence of proinflammatory stimuli. Cellular inflammation was induced by treatment with lipopolysaccharide (LPS) or the cytokine, interleukin 1 beta (IL-1β). In a separate set of experiments, cells were pretreated with IL-1ra prior to exposure to LPS or IL-1β. Prostaglandin E2 and leukotriene B4 (LTB4) levels were quantified by ELISA assays. Both LPS and IL-1β exposure were noted to stimulate cellular PGE2 release, a response which was significantly inhibited by IL-1ra treatment. Either stimulant when administered alone failed to stimulate release of LTB4. When administered after IL-1ra pretreatment however, both stimuli caused a significant increase in LTB4 release. These results suggest that a cytokine receptor antagonist can selectively influence eicosanoid production in this cell line. Furthermore, this study suggests that a IL-1ra may have a future clinical role in the treatment of inflammatory disorders of the colon which are intimately linked to enhanced eicosanoid synthesis.http://dx.doi.org/10.1155/S0962935196000622 |
| spellingShingle | G. S. Smith C. Rieckenberg W. E. Longo D. L. Kaminski J. E. Mazuski Y. Deshpande T. A. Miller The effect of an interleukin receptor antagonist (IL-1ra) on colonocyte eicosanoid release Mediators of Inflammation |
| title | The effect of an interleukin receptor antagonist (IL-1ra) on colonocyte eicosanoid release |
| title_full | The effect of an interleukin receptor antagonist (IL-1ra) on colonocyte eicosanoid release |
| title_fullStr | The effect of an interleukin receptor antagonist (IL-1ra) on colonocyte eicosanoid release |
| title_full_unstemmed | The effect of an interleukin receptor antagonist (IL-1ra) on colonocyte eicosanoid release |
| title_short | The effect of an interleukin receptor antagonist (IL-1ra) on colonocyte eicosanoid release |
| title_sort | effect of an interleukin receptor antagonist il 1ra on colonocyte eicosanoid release |
| url | http://dx.doi.org/10.1155/S0962935196000622 |
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