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Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice
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IL-38 Gene Deletion Worsens Murine Colitis.

Dennis M de Graaf1,2, Ruth X Wang3,4, Jesús Amo-Aparicio1

  • 1Department of Medicine, University of Colorado Denver, Aurora, CO, United States.

Frontiers in Immunology
|June 13, 2022
PubMed
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Interleukin-38 (IL-38) acts as an anti-inflammatory cytokine. Its deficiency exacerbates experimental colitis in mice by disinhibiting the NLRP3 inflammasome, suggesting a protective role in inflammatory bowel disease.

Keywords:
IBD – inflammatory bowel diseasesIL-1αIL-1βIL-38NLRP3colitis

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Area of Science:

  • Immunology
  • Gastroenterology
  • Cytokine Biology

Background:

  • Interleukin-38 (IL-38) is a recently identified cytokine within the IL-1 Family, primarily produced by B lymphocytes.
  • IL-38 possesses anti-inflammatory properties and plays a role in maintaining intestinal homeostasis.
  • Human studies suggest IL-38 may be protective against inflammatory bowel diseases (IBD) like ulcerative colitis and Crohn's disease.

Purpose of the Study:

  • To investigate the role of endogenous IL-38 in experimental colitis.
  • To determine the impact of IL-38 deficiency on colitis severity and associated inflammatory pathways in mice.

Main Methods:

  • Generation of IL-38 deficient mice by deleting exons 1-4.
  • Induction of experimental colitis using dextran sulfate sodium (DSS) in wild-type (WT) and IL-38 deficient mice.
  • Assessment of disease severity, intestinal permeability, histological damage, and inflammatory markers including NLRP3 inflammasome components, caspase-1, IL-1β, IL-1α, myeloperoxidase, and IL-17A/F.
  • Treatment of IL-38 deficient mice with an NLRP3 inhibitor.

Main Results:

  • IL-38 deficient mice exhibited exacerbated DSS-induced colitis, characterized by increased weight loss, intestinal permeability, and colonic neutrophil influx.
  • Absence of IL-38 led to elevated colonic NLRP3 mRNA and protein, increased caspase-1 activation, and heightened processing of IL-1β.
  • Expression of IL-1α, myeloperoxidase, IL-17a, and Il17f were upregulated in IL-38 deficient mice.
  • NLRP3 inhibition attenuated disease severity during the recovery phase in IL-38 deficient mice.

Conclusions:

  • Endogenous IL-38 functions as an anti-inflammatory cytokine that ameliorates DSS-induced colitis.
  • A relative deficiency in IL-38 may contribute to IBD pathogenesis by allowing NLRP3 inflammasome overactivation.
  • Targeting IL-38 or the NLRP3 inflammasome could represent potential therapeutic strategies for IBD.