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Lianna Zhou1, Zhaoqi Yan2, Wei Yang3

  • 1Department of Cell, Developmental and Integrative Biology, University of Alabama at Birmingham, Birmingham, AL, United States.

Frontiers in Immunology
|June 7, 2023
PubMed
Summary
This summary is machine-generated.

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Mice lacking Suppressors Of Cytokine Signaling 3 (Socs3) in myeloid cells experienced worsened inflammatory bowel disease (IBD). Socs3 deficiency enhanced neutrophil activation, suggesting it protects against IBD by regulating immune responses.

Area of Science:

  • Immunology
  • Gastroenterology
  • Molecular Biology

Background:

  • Myeloid cells are key players in Inflammatory Bowel Diseases (IBD), such as Ulcerative Colitis and Crohn's Disease.
  • The JAK/STAT pathway, regulated by Suppressors Of Cytokine Signaling (SOCS) proteins, is implicated in IBD pathogenesis.
  • Previous research linked myeloid cell SOCS3 deficiency to hyperactivated immune cells in a Multiple Sclerosis model.

Purpose of the Study:

  • To investigate the role of myeloid cell SOCS3 in the development of colitis.
  • To understand how SOCS3 deficiency in myeloid cells impacts immune cell function and disease severity in a colitis model.

Main Methods:

  • Utilized a DSS-induced colitis model in mice with myeloid cell-specific Socs3 deletion (Socs3 ΔLysM).
  • Analyzed immune cell infiltration in the colon and spleen.
Keywords:
inflammatory bowel diseases (IBDs)myeloid cellsneutrophilssuppressors of cytokine signaling (SOCS)ulcerative colitis (uc)

Related Experiment Videos

  • Assessed gene expression in monocytes and neutrophils.
  • Depleted neutrophils using anti-Ly6G antibody to evaluate their role in disease severity.

    • Main Results:

    • Socs3 deficiency in myeloid cells exacerbated DSS-induced colitis.
    • Increased infiltration of monocytes and neutrophils was observed in the colon and spleen of Socs3-deficient mice.
    • Genes associated with colitis pathogenesis (Il1β, Lcn2, S100a8, S100a9) were upregulated in Socs3-deficient neutrophils.
    • Neutrophil depletion significantly ameliorated colitis severity in Socs3-deficient mice.

    Conclusions:

    • Myeloid cell SOCS3 deficiency exacerbates DSS-induced colitis by promoting neutrophil activation and infiltration.
    • SOCS3 acts as a crucial regulator preventing excessive immune activation in IBD.
    • Targeting neutrophil hyperactivation in SOCS3-deficient individuals may offer novel therapeutic strategies for IBD.