2084 ANTI-INFLAMMATORY M2 MACROPHAGES SUPPRESS RENAL CRYSTAL FORMATION VIA A COLONY STIMULATING FACTOR-1 DEPENDENT PATHWAY IN M2-DEFICIENT (OP/OP) MICE

2013 ◽  
Vol 189 (4S) ◽  
Author(s):  
Kazumi Taguchi ◽  
Atsushi Okada ◽  
Takahiro Yasui ◽  
Kazuhiro Niimi ◽  
Yasuhiro Fujii ◽  
...  
Keyword(s):  
Crystal Formation ◽  
M2 Macrophages ◽  
Colony Stimulating Factor ◽  
Anti Inflammatory ◽  
Stimulating Factor ◽  
Dependent Pathway

scholarly journals Multiple signaling pathways induced by granulocyte colony-stimulating factor involving activation of JAKs, STAT5, and/or STAT3 are required for regulation of three distinct classes of immediate early genes

Blood ◽  
1996 ◽  
Vol 88 (12) ◽  
pp. 4435-4444 ◽  
Author(s):  
SS Tian ◽  
P Tapley ◽  
C Sincich ◽  
RB Stein ◽  
J Rosen ◽  
...  
Keyword(s):  
Immediate Early Genes ◽  
Signaling Molecules ◽  
Immediate Early ◽  
Terminal Deletion ◽  
Deletion Mutants ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Multiple Signaling ◽  
Stimulating Factor ◽  
Dependent Pathway

Granulocyte colony-stimulating factor (G-CSF) is the major regulator of proliferation and differentiation of neutrophilic granulocyte precursor cells. G-CSF activates multiple signaling molecules, including the JAK1 and JAK2 kinases and the STAT transcription factors. To investigate G-CSF signaling events regulated by the JAK-STAT pathway, we have generated UT7-epo cells stably expressing either wild-type (wt) G-CSF receptor or a series of C-terminal deletion mutants. Gel mobility shift and immunoprecipitation/Western analysis showed that STAT5 is rapidly activated by G-CSF in cells expressing the wt G-CSF receptor, in addition to the previously reported STAT3 and STAT1. Mutants lacking any tyrosine residues in the cytoplasmic domain maintain their ability to activate STAT5 and STAT1 but cannot activate STAT3, implying that STAT5 and STAT1 activation does not require receptor tyrosine phosphorylation. We also observed significant changes in the ratio of STAT1:STAT3:STAT5 activated by various G-CSF receptor C-terminal deletion mutants. These mutant receptors were further used to investigate the role of JAKs and STATs in G-CSF-mediated responses in these cells. We found that JAK activation correlates with G-CSF-induced cell proliferation, whereas STAT activation is not required. We have also identified three classes of G-CSF immediate early genes, whose activation correlates with the activation of distinct JAK-STAT pathways. Our data show that, whereas c-fos is regulated through a pathway independent of STAT activation, oncostatin M, IRF-1, and egr-1 are regulated by an STAT5-dependent pathway and fibrinogen is regulated by an STAT3-dependent pathway. In conclusion, our results suggest that G-CSF regulates its complex biologic activities by selectively activating distinct early response genes through different JAK-STAT signaling molecules.

Anti-inflammatory effects of resveratrol in lung epithelial cells: molecular mechanisms

2004 ◽  
Vol 287 (4) ◽  
pp. L774-L783 ◽  
Author(s):  
Louise E. Donnelly ◽  
Robert Newton ◽  
Gina E. Kennedy ◽  
Peter S. Fenwick ◽  
Rachel H. F. Leung ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
A549 Cells ◽  
Airway Epithelial Cells ◽  
Airway Epithelial ◽  
Colony Stimulating Factor ◽  
Macrophage Colony Stimulating Factor ◽  
Anti Inflammatory ◽  
Macrophage Colony ◽  
Stimulating Factor ◽  
Factor Release

Resveratrol (3,4′,5-trihydroxystilbene) is a polyphenolic stilbene found in the skins of red fruits, including grapes, that may be responsible for some of the health benefits ascribed to consumption of red wine. Resveratrol has been shown to have antioxidant properties and can act as an estrogen agonist. This study examined the anti-inflammatory effects of resveratrol on human airway epithelial cells. Resveratrol and the related molecule quercetin, but not deoxyrhapontin, inhibited IL-8 and granulocyte-macrophage colony-stimulating factor release from A549 cells. Neither the estrogen receptor antagonist tamoxifen nor the glucocorticoid antagonist mifepristone altered the inhibitory effect of resveratrol. The mechanism of resveratrol action was investigated further using luciferase reporter genes stably transfected into A549 cells. Resveratrol and quercetin inhibited NF-κB-, activator protein-1-, and cAMP response element binding protein-dependent transcription to a greater extent than the glucocorticosteroid dexamethasone. These compounds also had no significant effect on acetylation or deacetylation of core histones. Resveratrol, but not estradiol or N-acetyl cysteine, inhibited cytokine-stimulated inducible nitric oxide synthase expression and nitrite production (IC50 = 3.6 ± 2.9 μM) in human primary airway epithelial cells. Resveratrol also inhibited granulocyte-macrophage colony-stimulating factor release (IC50 = 0.44 ± 0.17 μM), IL-8 release (IC50 = 4.7 ± 3.3 μM), and cyclooxygenase-2 expression in these cells. This study demonstrates that resveratrol and quercetin have novel nonsteroidal anti-inflammatory activity that may have applications for the treatment of inflammatory diseases.

Drug-induced agranulocytosis (clinical observation)

2021 ◽  
Vol 1 (30) ◽  
pp. 19-23
Author(s):  
N. A. Sokolova ◽  
L. V. Pozdnyakova ◽  
I. S. Tatarinova
Keyword(s):  
Adverse Effect ◽  
Clinical Observation ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Drug Induced ◽  
Life Threatening ◽  
Inflammatory Drugs ◽  
Anti Inflammatory ◽  
Antithyroid Agents ◽  
Stimulating Factor

The majority of agranulocytosis cases are caused by drugs, including nonsteroidal anti-inflammatory drugs, antibiotics, antithyroid agents, etc. Here, we report a case of severe agranulocytosis in a 67-year-old woman following nonsteroidal anti-inflammatory therapy which was successfully managed using recombinant human granulocyte colony-stimulating factor. Although metamizole, has been in use since 1922 in the management of postoperative pain, colic pain, cancer pain and migraine, agranulocytosis as a direct side effect of metamizole therapy has been rarely reported. It is important to keep in mind this rare but potentially life-threatening adverse effect of metamizole, when initiating therapy.

scholarly journals Anti-Inflammatory Effects of Diospyrin on Lipopolysaccharide-Induced Inflammation Using RAW 264.7 Mouse Macrophages

Biomedicines ◽  
2020 ◽  
Vol 8 (1) ◽  
pp. 11 ◽  
Author(s):  
Adnan Shahidullah ◽  
Ji-Young Lee ◽  
Young-Jin Kim ◽  
Syed Muhammad Ashhad Halimi ◽  
Abdur Rauf ◽  
...  
Keyword(s):  
Leishmania Donovani ◽  
Calcium Release ◽  
Tumor Necrosis Factor Receptor ◽  
Mitogen Activated Protein Kinase ◽  
Raw 264.7 Cells ◽  
Raw 264.7 ◽  
Colony Stimulating Factor ◽  
Mouse Macrophages ◽  
Anti Inflammatory ◽  
Stimulating Factor

Diospyrin is a bisnaphthoquinonoid medicinal compound derived from Diospyros lotus, with known anti-cancer, anti-tubercular, and anti-leishmanial activities against Leishmania donovani. However, the effects of diospyrin on lipopolysaccharide (LPS)-induced macrophage activation and inflammation are not fully reported. In this study, the anti-inflammatory effects of diospyrin on LPS-induced macrophages were examined. Diospyrin showed no toxicity in RAW 264.7 at concentrations of up to 10 μM. Diospyrin moderated the production of nitric oxide (NO), monocyte chemotactic protein-1, macrophage inflammatory protein-1β, interleukin (IL)-6, IL-10, granulocyte colony-stimulating factor, granulocyte macrophage colony-stimulating factor, vascular endothelial growth factor, leukemia inhibitory factor, and RANTES/CCL5, as well as calcium release in LPS-induced RAW 264.7, at concentrations of up to 10 μM significantly (p < 0.05). Diospyrin also significantly inhibited the phosphorylation of p38 mitogen-activated protein kinase (MAPK) and mRNA expression of C/EBP homologous protein (CHOP), as well as tumor necrosis factor receptor superfamily member 6 (Fas), in LPS-induced RAW 264.7 cells at concentrations of up to 10 μM (p < 0.05). Diospyrin exhibits anti-inflammatory properties mediated via inhibition of NO, and cytokines in LPS-induced mouse macrophages via the ER-stressed calcium-p38 MAPK/CHOP/Fas pathway.

scholarly journals Colony-Stimulating Factor-1 Signaling Suppresses Renal Crystal Formation

2014 ◽  
Vol 25 (8) ◽  
pp. 1680-1697 ◽  
Author(s):  
Kazumi Taguchi ◽  
Atsushi Okada ◽  
Hiroshi Kitamura ◽  
Takahiro Yasui ◽  
Taku Naiki ◽  
...  
Keyword(s):  
Crystal Formation ◽  
Colony Stimulating Factor ◽  
Stimulating Factor
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