Iloprost Affects Macrophage Activation and CCL2 Concentrations in a Microdialysis Model in Rats

Alkhatib, Kamel; Poseno, Tina M.; Perez, Alda Diaz; Durdik, Jeannine M.; Stenken, Julie A.

doi:10.1007/s11095-017-2277-1

Cited by 3 publications

(2 citation statements)

References 38 publications

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“…This finding was further confirmed by the increase of the pro-regenerative M2 type macrophages under the influence of Iloprost. The group of Alkhabit also showed an immune modulatory effect of Iloprost on macrophage polarization toward a pro-regenerative phenotype in an in vivo model system in rats, supporting our findings (33). Regarding bone fracture healing, possible negative effects of Iloprost on MSCs and bone forming osteoblasts as well as bone resorbing osteoclasts have to be considered.…”

Section: Discussionsupporting

confidence: 89%

Immune Modulation to Enhance Bone Healing—A New Concept to Induce Bone Using Prostacyclin to Locally Modulate Immunity

et al. 2019

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Within an aging population, fracture incidences will rise and with the augmented risks of impaired healing the overall risk of delayed bone regeneration will substantially increase in elderly patients. Thus, new strategies to rescue fracture healing in the elderly are highly warranted. Modulating the initial inflammatory phase toward a reduced pro-inflammation launches new treatment options for delayed or impaired healing specifically in the elderly. Here, we evaluated the capacity of the prostacyclin analog Iloprost to modulate the inflammatory phase toward a pro-regenerative milieu using in vitro as well as in vivo model systems. In vitro , Iloprost administration led to a downregulation of potential unfavorable CD8+ cytotoxic T cells as well as their pro-inflammatory cytokine secretion profile. Furthermore, Iloprost increased the mineralization capacity of osteogenic induced mesenchymal stromal cells through both direct as well as indirect cues. In an in vivo approach, Iloprost, embedded in a biphasic fibrin scaffold, decreased the pro-inflammatory and simultaneously enhanced the anti-inflammatory phase thereby improving bone healing outcome. Overall, our presented data confirms a possible strategy to modulate the early inflammatory phase in aged individuals toward a physiological healing by a downregulation of an excessive pro-inflammation that otherwise would impair healing. Further confirmation in phase I/II trials, however, is needed to validate the concept in a broader clinical evaluation.

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Section: Discussionsupporting

confidence: 89%

Immune Modulation to Enhance Bone Healing—A New Concept to Induce Bone Using Prostacyclin to Locally Modulate Immunity

et al. 2019

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“…We believe that, the NLRP3 inflammasome has a direct regulatory effect on MCP-1 transcription that is independent of IL-1β, which is very important because many studies have demonstrated the important role of MCP-1 in the macrophage polarization towards the M1 phenotype and in impairment of cardiac function. [27][28][29] Notably, the role of MCP-1 in driving the direction of macrophage polarization has been controversial in many nonheart disease studies. [30][31][32][33][34][35][36] However, in studies related to cardiovascular disease and heart failure, the role of the MCP-1-CCR2 pathway in promoting M1 polarization and the proinflammatory effect of CCR2 + macrophages have been more widely reported, [37][38][39][40][41][42][43] which is consistent with our experimental results.…”

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confidence: 99%

Regulation of the Immune Microenvironment by an NLRP3 Inhibitor Contributes to Attenuation of Acute Right Ventricular Failure in Rats with Pulmonary Arterial Hypertension

Guo¹,

Qin²,

Cao³

et al. 2021

JIR

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Exosome miR-155-5p Derived from Lung Cancer Hcc827 Promotes Macrophage Activation and Lung Cancer Progression

Wang

Luo

et al. 2022

j biomater tissue eng

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This stud intends to assess whether exosome miR-155-5p derived from human non-small cell lung cancer cells (Hcc827) activates macrophages in lung cancer. Lung cancer Hcc827 cells were assigned into control group and expeirmental group (cultured with macrophages, THP-1 activated by exosome miR-155-5P derived from Hcc827) followed by analysis of macrophage markers inducible nitric oxide synthase (INOS), recombinant human CD163 (CD163), matrix metallopeptidase 9 (MMP9), matrix metallopeptidase 2 (MMP2), and E-cadherin by real-time fluorescent quantitative PCR (RFQ-PCR), IL-10, IL-6 and IL-8 levels by chemiluminescence, cell invasion by Transwell assay and related protein expression by Western blot. miR-155-5p treatment significantly reduced INOS and TNF-β expressions and increased CD163, TNF-α, IL-8, IL-6 and IL-10 expressions along with enhanced cell invasion. In addition, MMP9 and MMP2 expressions in experimental group were significantly increased and E-cdherin was reduced. In conclusion, exosome miR-155-5p derived from lung cancer Hcc827 cells activates macrophages and enhanced lung cancer cell invasion.

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Iloprost Affects Macrophage Activation and CCL2 Concentrations in a Microdialysis Model in Rats

Abstract: Localized delivery of iloprost caused macrophage activation at the tissue interface of a microdialysis subcutaneous implant in rat. This model system may be useful for testing other potential macrophage modulators in vivo.

Cited by 3 publications

References 38 publications

Immune Modulation to Enhance Bone Healing—A New Concept to Induce Bone Using Prostacyclin to Locally Modulate Immunity

Immune Modulation to Enhance Bone Healing—A New Concept to Induce Bone Using Prostacyclin to Locally Modulate Immunity

Regulation of the Immune Microenvironment by an NLRP3 Inhibitor Contributes to Attenuation of Acute Right Ventricular Failure in Rats with Pulmonary Arterial Hypertension

Exosome miR-155-5p Derived from Lung Cancer Hcc827 Promotes Macrophage Activation and Lung Cancer Progression

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