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Toll-like receptor expression and function in type I bipolar disorder.

Andrea Wieck1, Rodrigo Grassi-Oliveira2, Carine Hartmann do Prado3

  • 1Laboratory of Immunosenescence, Institute of Biomedical Research, Pontifical Catholic University of the Rio Grande do Sul (PUCRS), Porto Alegre, Brazil; Postgraduate Program in Biomedical Gerontology, Brazil.

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Bipolar disorder (BD) involves immune imbalance. This study found altered Toll-like receptor (TLR) expression and signaling in BD patients, suggesting a role in inflammation.

Keywords:
Bipolar disorderInflammationInnate immunityMonocytesRegulatory T cellsToll-like receptors

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Area of Science:

  • Immunology
  • Neuroscience
  • Cell Biology

Background:

  • Bipolar disorder (BD) is linked to immune dysregulation and chronic low-grade inflammation.
  • The precise cellular and molecular mechanisms driving this inflammation in BD are not fully understood.
  • Toll-like receptors (TLRs), crucial in immune cell signaling, are potential mediators of these inflammatory processes.

Purpose of the Study:

  • To investigate the expression and function of Toll-like receptors (TLRs) 1, 2, 4, 5, and 6 in immune cells of bipolar disorder patients.
  • To explore the association between TLR signaling pathways and the inflammatory profile in euthymic individuals with type I BD.

Main Methods:

  • Flow cytometry was used to analyze TLR expression on monocytes, regulatory T cells (Tregs), and activated T cells from BD patients and healthy controls (HCs).
  • Monocytes were stimulated in vitro with specific TLR agonists.
  • Cytokine levels (IL-8, IL-1β, IL-6, IL-10, TNF-α, IL-12p70) were quantified using cytometric bead arrays.

Main Results:

  • BD patients exhibited higher baseline percentages of TLR-1+ and TLR-2+ monocytes, with reduced TLR-5 expression compared to HCs.
  • Following TLR agonist stimulation, BD monocytes showed increased percentages of TLR-1+, TLR-2+, and TLR-6+ cells.
  • Elevated levels of IL-8, IL-12p70, and TNF-α were observed in BD patients after stimulation, indicating enhanced TLR signaling.
  • Increased TLR-2+ Tregs and TLR-2+/TLR-5+ activated T cells were noted in BD patients.

Conclusions:

  • The findings suggest dysregulated Toll-like receptor (TLR) expression and heightened signaling in immune cells of bipolar disorder patients.
  • These TLR alterations may contribute to the observed low-grade inflammatory state associated with BD.
  • TLRs represent a potential therapeutic target for managing immune dysregulation in bipolar disorder.