The activation of monocyte and T cell networks in patients with bipolar disorder
Objectives: We recently described a monocyte pro-inflammatory state in patients with bipolar disorder (BD). We hypothesized that the CD4+T cell system is also activated and determined percentages of Th1, Th2, Th17 and CD4+CD25highFoxP3+regulatory T cells. Methods: We carried out a detailed FACS analysis to determine the various T cell subsets and used frozen stored peripheral blood mononuclear cells (PBMC) of 38 BD patients (of whom we previously had tested monocytes for pro-inflammatory gene expression (Drexhage et al., 2010b; Padmos et al., 2008)) and of 22. age/gender matched healthy controls (HC). In addition the cytokines CCL2, IL-1β, IL-6, TNF-α, PTX3, IL-10, IFN-γ, IL-17A, IL-4, IL-5 and IL-22 were measured in serum. Results: (a) Serum sCD25 levels and percentages of anti-inflammatory CD4+CD25highFoxP3+ regulatory T cells were higher, the latter in BD patients <40years of age. Percentages of Th1, Th2 and Th17 cells were normal.(b) Of the pro-inflammatory monocyte cytokines CCL2 and PTX3 were raised in serum.(c) The monocyte pro-inflammatory state and the raised percentages of CD4+CD25highFoxP3+regulatory T cells occurred independently from each other.(d) In BD patients positive for thyroid autoimmune disease a significantly reduced percentage of CD4+CD25highFoxP3+regulatory T cells was found as compared to BD patients without AITD. Conclusion: Our data show an enhancement of pro-inflammatory monocyte and anti-inflammatory T cell forces in BD patients. A lack of anti-inflammatory T cell forces co-occurred with AITD in BD patients.
|Keywords||Activated inflammatory response system, Bipolar disorder, FACS, Regulatory T cells, Thyroid autoimmunity|
|Persistent URL||dx.doi.org/10.1016/j.bbi.2011.03.013, hdl.handle.net/1765/33952|
Drexhage, R.C, Hoogenboezem, T.H, Versnel, M.A, Berghout, A, & Nolen, W.A. (2011). The activation of monocyte and T cell networks in patients with bipolar disorder. Brain, Behavior, and Immunity, 25(6), 1206–1213. doi:10.1016/j.bbi.2011.03.013