ArticleMediators of inflammation2013
Inflammatory mediator profiling reveals immune properties of chemotactic gradients and macrophage mediator production inhibition during thioglycollate elicited peritoneal inflammation.
Article in Mediators of inflammation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 42 citations in OpenAlex.
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- Exploring the complex immunomodulatory effects and gut defense via oral administration of Astragali radix water extract to normal mice.BMC complementary medicine and therapies · 2024Article
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- Menstrual blood-derived stromal cells modulate functional properties of mouse and human macrophages.Scientific reports · 2020Article
- Soluble PD-L1 improved direct ARDS by reducing monocyte-derived macrophages.Cell death & disease · 2020Article
- Arctigenin protects mice from thioglycollate-induced acute peritonitis.Pharmacology research & perspectives · 2020Article
- Deriving a Boolean dynamics to reveal macrophage activation with in vitro temporal cytokine expression profiles.BMC bioinformatics · 2019Article
- Macrophages from Mice AdministeredNutrients · 2018Article
- Improvement of Adipose Macrophage Polarization in High Fat Diet-Induced Obese GHSR Knockout Mice.BioMed research international · 2018Article
- Soluble ectodomain CD163 and extracellular vesicle-associated CD163 are two differently regulated forms of 'soluble CD163' in plasma.Scientific reports · 2017Article
- Mesenchymal Stromal Cell-Derived Microvesicles Regulate an Internal Pro-Inflammatory Program in Activated Macrophages.Frontiers in immunology · 2017Article
- Absence of the Non-Signalling Chemerin Receptor CCRL2 Exacerbates Acute Inflammatory ResponsesFrontiers in immunology · 2017Article
- Toll-Like Receptor Ligands and Interferon-γ Synergize for Induction of Antitumor M1 Macrophages.Frontiers in immunology · 2017Article
- Oncostatin M binds to extracellular matrix in a bioactive conformation: implications for inflammation and metastasis.Cytokine · 2015Article
- Bone marrow from blotchy mice is dispensable to regulate blood copper and aortic pathologies but required for inflammatory mediator production in LDLR-deficient mice during chronic angiotensin II infusion.Annals of vascular surgery · 2015Article
- Counteract of bone marrow of blotchy mice against the increases of plasma copper levels induced by high-fat diets in LDLR-/- mice.Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS) · 2015Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Understanding of spatiotemporal profiling of inflammatory mediators and their associations with MΦ accumulation is crucial to elucidate the complex immune properties. Here, we used murine thioglycollate elicited peritonitis to determine concentrations of 23 inflammatory mediators in peritoneal exudates and plasma before (day 0) and after (days 1 and 3) thioglycollate administration to peritoneal cavities; these mediators included TNF-α , FGF-9, IFN-γ , IP-10, RANTES, IL-1α , IL-6, IL-7, IL-10, IL-11, IL-12p70, IL-17A, lymphotactin, OSM, KC/GRO, SCF, MIP-1β , MIP-2, TIMP-1, VEGF-A, MCP-1, MCP-3, and MCP-5. Our results showed that concentrations of most mediators in exudates and plasma reached peak levels on day 1 and were significantly reduced on day 3. Conversely, MΦ numbers started to increase on day 1 and reached peak levels on day 3. Moreover, LPS treatment in vitro significantly induced mediator productions in cell culture media and lysates from MΦ isolated on day 3. Our results also showed that on day 0, concentrations of many mediators in plasma were higher than those in exudates, whereas on day 1, the trend was reversed. Overall, the findings from thioglycollate elicited peritonitis reveal that reversible chemotactic gradients between peritoneal exudates and blood exist in basal and inflamed conditions and the inflammatory mediator production in vivo is disassociated with macrophage accumulation during inflammation resolution.
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