ArticleScientific reports2017
CSF-1 regulates the function of monocytes in Crohn's disease patients in remission.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- Identification of platelet-related subtypes and diagnostic markers in pediatric Crohn's disease based on WGCNA and machine learning.Frontiers in immunology · 2024Article
- Selected Cytokines and Metalloproteinases in Inflammatory Bowel Disease.International journal of molecular sciences · 2023Review
- Colon Expression of Chemokines and Their Receptors Depending on the Stage ofInternational journal of molecular sciences · 2022Article
- Article
- Blocking the CCL5-CCR5 Axis Using Maraviroc Promotes M1 Polarization of Macrophages Cocultured with Irradiated Hepatoma Cells.Journal of hepatocellular carcinoma · 2021Article
- Multi-parameter immune profiling of peripheral blood mononuclear cells by multiplexed single-cell mass cytometry in patients with early multiple sclerosis.Scientific reports · 2019Article
- Function of CSF1 and IL34 in Macrophage Homeostasis, Inflammation, and Cancer.Frontiers in immunology · 2019Article
- Preclinical evaluation of EPHX2 inhibition as a novel treatment for inflammatory bowel disease.PloS one · 2019Article
- Origin, Differentiation, and Function of Intestinal Macrophages.Frontiers in immunology · 2018Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During the flare-ups of Crohn's disease (CD) patients, circulating leukocytes actively migrate toward the inflamed sites. During the remission, the lack of symptoms does not necessarily imply immunological remission. To decipher inflammatory mechanisms still operating during CD remission, we compared the expression of chemokine receptors on monocytes from CD and healthy donors (HD), and how these differences could modulate monocyte maturation and cytokine production. Flow cytometry analysis showed a higher expression of CCR5 on monocytes from CD patients than those from HD after 24 h. This CCR5 upregulation was associated with the spontaneous production of CSF-1 and IL-10. The higher expression of CCR5 on CD monocytes increased their migratory pattern in response to CCL5. Signaling through CCR5/CCL5 increased CD163 and HLA-DR expression and diminished TLR4-induced TNF-α and IL-6 secretion during monocyte differentiation. When we analyzed clinical parameters, patients treated with azathioprine had the highest CSF-1 levels and CCR5 expression. Our results suggest that monocytes from CD patients in remission produced high levels of CSF-1 that upregulate CCR5 expression. Consequently, monocytes differentiated in these conditions had a characteristic phenotype and lower production of inflammatory cytokines. The treatment with azathioprine could be responsible for this anti-inflammatory profile of monocytes.
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