The DOI matches its Crossref record; 56 of the 56 references it cites were found in a registry or an index.
Neutralization of interleukin-18 reduces severity in murine colitis and intestinal IFN-γ and TNF-α production
Abstract
Interleukin (IL)-18, initially described as interferon (IFN)-γ-inducing factor, is expressed in the inflamed mucosa of patients with Crohn's disease. To investigate the role of IL-18 in intestinal inflammation, the effect of neutralizing antimurine IL-18 antiserum in dextran sulfate sodium (DSS)-induced colitis in BALB/c and C57BL/6 mice was examined. During a dose response of DSS, levels of colonic IL-18 increased parallel with clinical worsening. With the use of confocal laser microscopy, the increased IL-18 was localized to the intestinal epithelial layer. Anti-IL-18 treatment resulted in a dose-dependent reduction of the severity of colitis in both BALB/c and C57BL/6 mice. Colon shortening following DSS-induced colitis was partially prevented in the treatment groups. In the colon tissue homogenates, IFN-γ concentrations were lower in the anti-IL-18-treated DSS-fed mice compared with untreated DSS-fed mice. This suppressive effect of anti-IL-18 administered in vivo was also observed on spontaneous tumor necrosis factor-α, IL-18, and IFN-γ production from ex vivo colon organ cultures. The stimulation of lamina propria mononuclear cells by IL-18 and IL-12 resulted in a synergistic increase in IFN-γ synthesis. These findings suggest that IL-18 is a pivotal mediator in experimental colitis.
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Cites
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Cited by
Cytokines in inflammatory bowel disease
Neurath, M. F. (2014) · Nature Reviews Immunology · doi:10.1038/nri3661 · Cited by 2,706
The interleukin-1 family: back to the future
Garlanda, C., Dinarello, C. A., & Mantovani, A. (2013) · Immunity · doi:10.1016/j.immuni.2013.11.010 · Cited by 1,945
“Induction of IFN-g by IL-18 requires caspase-1 processing (Siegmund et al., 2001b).”
Overview of the IL ‐1 family in innate inflammation and acquired immunity
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Molecular Mechanisms RegulatinG Th1 Immune Responses
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Metadata
- Authors
- Siegmund, B., Fantuzzi, G., Rieder, F., Gamboni-Robertson, F., Lehr, H.-A., Hartmann, G., Dinarello, C. A., Endres, S., & Eigler, A.
- Venue
- American Journal of Physiology-Regulatory, Integrative and Comparative Physiology
- Publisher
- American Physiological Society
- Published
- 2001-10-01
- Volume
- 281
- Issue
- 4
- Pages
- R1264-R1273
- ISSN
- 0363-6119 (ISSN-L)
- 1522-1490
- OpenAlex
- W2098711659
- Cited by
- 288
- References
- 56
- FWCI
- 8.11
- Type
- journal article
- Language
- en
- Open access
- closed
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- Siegmund, B., Fantuzzi, G., Rieder, F., Gamboni-Robertson, F., Lehr, H.-A., Hartmann, G., Dinarello, C. A., Endres, S., & Eigler, A. (2001). Neutralization of interleukin-18 reduces severity in murine colitis and intestinal IFN-γ and TNF-α production. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology. https://doi.org/10.1152/ajpregu.2001.281.4.r1264
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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