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(+)CD25(high)FoxP3(+) 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(+)CD25(high)FoxP3+ regulatory T cells were higher, the latter in BD patients <40 years 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(+)CD25(high)FoxP3(+) regulatory T cells occurred independently from each other. (d) In BD patients positive for thyroid autoimmune disease a significantly reduced percentage of CD4(+)CD25(high)FoxP3(+) 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.
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(+)CD25(high)FoxP3(+) 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 BDpatients (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(+)CD25(high)FoxP3+ regulatory T cells were higher, the latter in BDpatients <40 years 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(+)CD25(high)FoxP3(+) regulatory T cells occurred independently from each other. (d) In BDpatients positive for thyroid autoimmune disease a significantly reduced percentage of CD4(+)CD25(high)FoxP3(+) regulatory T cells was found as compared to BDpatients without AITD. CONCLUSION: Our data show an enhancement of pro-inflammatory monocyte and anti-inflammatory T cell forces in BDpatients. A lack of anti-inflammatory T cell forces co-occurred with AITD in BDpatients.
Authors: Emily G Severance; Kristin L Gressitt; Shuojia Yang; Cassie R Stallings; Andrea E Origoni; Crystal Vaughan; Sunil Khushalani; Armin Alaedini; Faith B Dickerson; Robert H Yolken Journal: Bipolar Disord Date: 2013-12-06 Impact factor: 6.744
Authors: Barry McGuiness; Sinead M Gibney; Wouter Beumer; Marjan A Versnel; Inge Sillaber; Andrew Harkin; Hemmo A Drexhage Journal: Neuroimmunomodulation Date: 2016-08-17 Impact factor: 2.492
Authors: Michael Maes; Joao Victor Nani; Cristiano Noto; Lucas Rizzo; Mirian A F Hayashi; Elisa Brietzke Journal: Mol Neurobiol Date: 2020-09-11 Impact factor: 5.590