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Published on: August 12, 2019
Monocyte/macrophage mediates the impact of depression on Crohn's disease
Xin Zhang1, Pengbo Wang2, Yi Yang1
1Department of Gastroenterology, West China Hospital, Sichuan University, Chengdu, People's Republic of China.
Insights
Depression negatively impacts Crohn's disease (CD) by altering monocytes/macrophages. These immune cells show reduced phagocytosis and increased inflammation, worsening CD prognosis.
Area of Science:
- Immunology
- Gastroenterology
- Psychiatry
Background:
- Depression is linked to increased Crohn's disease (CD) risk and poorer outcomes.
- Monocytes and macrophages are key immune cells involved in both depression and CD pathogenesis.
Purpose of the Study:
- To investigate if monocytes/macrophages mediate depression's effect on CD.
- To examine alterations in monocyte/macrophage phagocytosis and cytokine production.
- To assess the impact on CD4+ T lymphocyte differentiation and intestinal epithelial barrier function.
Main Methods:
- Isolated monocytes/macrophages from CD patients (depressed vs. non-depressed).
- Assessed phagocytosis, cytokine production (TNF-α, IL-6, IL-1β), and T cell subset differentiation (Th1, Th2, Th17, Treg).
- Evaluated epithelial barrier integrity (Caco-2 cells) and tight junction protein expression.
Main Results:
- Depressed CD patients showed decreased monocyte/macrophage phagocytosis and elevated pro-inflammatory cytokines (TNF-α, IL-6, IL-1β).
- Monocytes from depressed patients promoted Th1/Th17 differentiation and suppressed Treg cells.
- Macrophages from depressed patients impaired epithelial barrier function, reducing TEER and tight junction proteins.
Conclusions:
- Monocyte/macrophage dysfunction contributes to depression's negative impact on CD.
- Mechanisms include reduced phagocytosis, increased inflammation, skewed T cell differentiation, and compromised epithelial barrier integrity.
Background:
Depression increases the risk of Crohn's disease (CD) and worsens its prognosis. Monocytes/macrophages, immune modulate cells, play vital roles in both depression and CD.
Objectives:
We investigated whether monocyte/macrophage could mediate the impact of depression on CD through induction of CD4 + T lymphocyte differentiation and epithelial barrier dysfunction, in addition to the alteration of their own phagocytic ability and cytokines production.
Methods:
Circulating monocytes and intestinal macrophages were isolated from eligible CD patients, divided into depressed and non-depressed groups. Phagocytosis was determined using flow cytometry while in vitro cytokine production was quantified using Luminex assay and qPCR. CD4 + T cells were cocultured with monocytes, then Type 1 Helper T Lymphocytes Th1/Type 2 Helper T Lymphocytes (Th2) /Type 17 Helper T Lymphocytes (Th17)/Treg subsets were analyzed using flow cytometry and qPCR. Caco-2 monolayers simulating epithelial barrier were cocultured with macrophages, and integrity and proliferation were evaluated. Tight junction protein expression was detected using immunofluorescence and western blot.
Results:
Decreased monocyte/macrophage phagocytosis and enhanced production of pro-inflammatory cytokines including Tumor necrosis factor-α (TNF-α), Interleukin-6 (IL-6) and Interleukin-1β (IL-1β) were revealed in the depressed versus non-depressed CD groups. Higher proportions of Th1 and Th17 cells with a lower proportion of Treg cell were observed after cocultured with monocytes from the depressed versus non-depressed CD patients. So were the expressions of their corresponding transcription factors T-bet, Retinoic Acid Related Orphan Nuclear Receptor gamma T (RORγt) and Forkhead box protein P3 (FoxP3). Caco-2 cells cocultured with macrophages from depressed CD displayed lower Transepithelial electric resistance (TEER), reduced proliferation activity, and decreased tight junction protein expressions compared with their counterpart cocultured with macrophages from non-depressed CD.
Conclusions:
Monocyte/macrophage may underlie the impact of depression upon CD via decreased phagocytosis, increased pro-inflammatory cytokine production, inducing CD4 + T cell differentiation toward Th1/Th17 cells rather than Treg cell, and impairing macrophage-enhanced epithelial barrier.
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