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Paradoxical effects of constitutive human IL-32{gamma} in transgenic mice during experimental colitis. | LitMetric

Paradoxical effects of constitutive human IL-32{gamma} in transgenic mice during experimental colitis.

Proc Natl Acad Sci U S A

Laboratory of Cytokine Immunology, Medical Immunology Center, Department of Bioscience and Biotechnology, School of Medicine, Konkuk University, Seoul 143-701, Korea.

Published: December 2010

AI Article Synopsis

  • Inflammatory cytokines play a crucial role in inflammatory bowel diseases, and therapies targeting these cytokines can help reduce disease severity.
  • A study using a transgenic mouse model expressing human IL-32γ showed early increased inflammation but ultimately less tissue damage and better survival rates after DSS-induced colitis, linked to higher IL-10 levels.
  • Elevated IL-32 levels were noted in humans with ulcerative colitis, suggesting IL-32γ may both contribute to inflammation and help protect intestinal integrity, depending on the context.

Article Abstract

Inflammatory cytokines mediate inflammatory bowel diseases (IBDs) and cytokine blocking therapies often ameliorate the disease severity. IL-32 affects inflammation by increasing the production of IL-1, TNFα, and several chemokines. Here, we investigated the role of IL-32 in intestinal inflammation by generating a transgenic (TG) mouse expressing human IL-32γ (IL-32γ TG). Although IL-32γ TG mice are healthy, constitutive serum and colonic tissue levels of TNFα are elevated. Compared with wild-type (WT) mice, IL-32γ TG mice exhibited a modestly exacerbated acute inflammation early following the initiation of dextran sodium sulfate (DSS)-induced colitis. However, after 6 d, there was less colonic inflammation, reduced tissue loss, and improved survival rate compared with WT mice. Associated with attenuated tissue damage, colonic levels of TNFα and IL-6 were significantly reduced in the IL-32γ TG mice whereas IL-10 was elevated. Cultured colon explants from IL-32γ TG mice secreted higher levels of IL-10 compared with WT mice and lower levels of TNFα and IL-6. Constitutive levels of IL-32γ itself in colonic tissues were significantly lower following DSS colitis. Although the highest level of serum IL-32γ occurred on day 3 of colitis, IL-32 was below constitutive levels on day 9. The ability of IL-32γ to increase constitutive IL-10 likely reduces TNFα, IL-6, and IL-32 itself accounting for less inflammation. In humans with ulcerative colitis (UC), serum IL-32 is elevated and colonic biopsies contain IL-32 in inflamed tissues but not in uninvolved tissues. Thus IL-32γ emerges as an example of how innate inflammation worsens as well as protects intestinal integrity.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3000248PMC
http://dx.doi.org/10.1073/pnas.1015418107DOI Listing

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