scholarly journals Lipopolysaccharides from Legionella and Rhizobium stimulate mouse bone marrow granulocytes via Toll-like receptor 2

2002 ◽  
Vol 116 (2) ◽  
pp. 293-302 ◽  
Author(s):  
R. Girard
Keyword(s):  
Bone Marrow ◽  
Mouse Bone Marrow ◽  
Toll Like Receptor ◽  
Toll Like Receptor 2 ◽  
Bone Marrow Granulocytes

scholarly journals Toll-Like Receptor Expression of Mesenchymal Stem Cells Derived from Granulocyte Colony-Stimulating Factor Treated Bone Marrow Donors

Acta Medica ◽  
2020 ◽  
Vol 51 (4) ◽  
pp. 33-40
Author(s):  
Tekin Aksu ◽  
Neslihan Karakurt ◽  
İrem Akar ◽  
Yasin Köksal ◽  
Fatih M. Azık ◽  
...  
Keyword(s):  
Stem Cells ◽  
Bone Marrow ◽  
Mesenchymal Stem Cells ◽  
Granulocyte Colony Stimulating Factor ◽  
Colony Stimulating Factor ◽  
Toll Like Receptor ◽  
Toll Like Receptors ◽  
Toll Like Receptor 2 ◽  
Stimulating Factor

Objective: The present study was planned to examine the expression of Toll-like receptors on human marrow-derived mesenchymal stem cells as a result of in-vivo exposure to granulocyte colony-stimulating factor with or without exposure of the cells to Toll-like receptors agonists. Materials and Methods: Toll-like receptor 2, 3, and 4 expressions of mesenchymal stem cells obtained from healthy human bone marrow donors exposed to in-vivo granulocyte colony-stimulating factor were analyzed, and granulocyte colony-stimulating factor untreated donors served as controls. Also, mesenchymal stem cells were stimulated in-vitro by Toll-like receptor agonists to observe the changes in the expression of the Toll-like receptors. Results: Mesenchymal stem cells obtained from both granulocyte colony-stimulating factor exposed or unexposed donors showed a low level of Toll-like receptor 2, 4 expressions by flow cytometry, whereas Toll-like receptor 3 expression was higher. Lipopolysaccharide was used as an agonist, but no significant difference was observed in the Toll-like receptor 2, 4 expressions, both in the granulocyte colony-stimulating factor exposed and unexposed groups. Stimulation of cells with Toll-like receptor 3 ligand was associated with a statistically significant decrease in Toll-like receptor 3 expressions, which was more profound in granulocyte colony-stimulating factor unexposed cells. Conclusion: We have shown that human bone marrow-derived culture-expanded mesenchymal stem cells express Toll-like receptor 3, whether in-vivo granulocyte colony-stimulating factor treated or untreated. Besides, the Toll-like receptor 3 agonist’s effect in lowering the expression levels was more significant in cells that were not exposed to granulocyte colony-stimulating factor. Additionally, detection of low expression of the pro-inflammatory Toll-like receptor 4 versus higher levels of Toll-like receptor 3 supports literature regarding the immunosuppressive characteristics of marrow-derived mesenchymal stem cells. Modulation of the expression of the Toll-like receptor of mesenchymal stem cells with granulocyte colony-stimulating factor or agonists may have implications in allogeneic mesenchymal stem cell therapies.

Arteriogenesis requires toll-like receptor 2 and 4 expression in bone-marrow derived cells

2011 ◽  
Vol 50 (1) ◽  
pp. 25-32 ◽  
Author(s):  
Daphne de Groot ◽  
Imo E. Hoefer ◽  
Sebastian Grundmann ◽  
Arjan Schoneveld ◽  
René T. Haverslag ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Toll Like Receptor ◽  
Bone Marrow Derived Cells ◽  
Toll Like Receptor 2

scholarly journals Effect of Chlamydia pneumoniae on Cellular ATP Content in Mouse Macrophages: Role of Toll-Like Receptor 2

2005 ◽  
Vol 73 (7) ◽  
pp. 4323-4326 ◽  
Author(s):  
Kambiz Yaraei ◽  
Lee Ann Campbell ◽  
Xiaodong Zhu ◽  
W. Conrad Liles ◽  
Cho-chou Kuo ◽  
...  
Keyword(s):  
Cell Death ◽  
Chlamydia Pneumoniae ◽  
Growth Cycle ◽  
Developmental Cycle ◽  
Mouse Bone Marrow ◽  
Atp Content ◽  
Toll Like Receptor ◽  
Mouse Macrophages ◽  
Toll Like Receptor 2 ◽  
In Cells

ABSTRACT Chlamydiae are obligate intracellular gram-negative bacteria and are dependent on the host cell for ATP. Thus, chlamydial infection may alter the intracellular levels of ATP and affect all energy-dependent processes within the cell. We have shown that both live C. pneumoniae and inactivated C. pneumoniae induce markers of cell death prior to completion of the bacterial growth cycle. As depletion of ATP could account for the observed increase in cell death, the effects of C. pneumoniae on ATP concentrations within mouse macrophages were investigated. Live, heat-killed, and UV-inactivated C. pneumoniae cultures (at multiplicities of infection [MOIs] of 0.01, 0.1, and 1.0) were incubated with mouse bone marrow macrophages isolated from C57BL/6J mice and mice deficient in Toll-like receptors. Treatment of the macrophages with both live and inactivated C. pneumoniae increased the ATP content of the cells. In cells infected with live C. pneumoniae, the increase was inversely proportional to the MOI. In cells treated with inactivated C. pneumoniae, the increase in ATP content was smaller than that induced by infection with live organisms and was proportional to the MOI. The increase in ATP content early in the developmental cycle was independent of the growth of C. pneumoniae, while sustained induction required live organisms. The capacity of C. pneumoniae to increase the ATP content was ablated in macrophages deficient in expression of either Toll-like receptor 2 or the Toll-like receptor accessory protein MyD88. In contrast, no effect was observed in macrophages lacking expression of Toll-like receptor 4.

scholarly journals Down-Modulation of L-Selectin by Lipopolysaccharide Is Not Required for Lipopolysaccharide-Induced Expression of CD14 in Mouse Bone Marrow Granulocytes

2001 ◽  
Vol 69 (7) ◽  
pp. 4287-4294 ◽  
Author(s):  
Thierry Pédron ◽  
Robert Girard ◽  
Richard Chaby
Keyword(s):  
Bone Marrow ◽  
Phorbol Ester ◽  
Polymorphonuclear Leukocytes ◽  
Cross Reactivity ◽  
Mouse Bone Marrow ◽  
Binding Studies ◽  
Induced Expression ◽  
Derivatives Of ◽  
Deficient Mice ◽  
Bone Marrow Granulocytes

ABSTRACT We established in previous studies that a constitutive lipopolysaccharide (LPS) receptor of low affinity is present on mouse bone marrow granulocytes (BMG). This yet-unidentified receptor is involved in the LPS-induced expression of a second LPS receptor, CD14. Because it has been claimed that L-selectin (CD62L) is a low-affinity LPS receptor in mature granulocytes (polymorphonuclear leukocytes), it may be asked whether this molecule could be the constitutive LPS receptor in BMG. We show in this study that l-selectin is constitutively present on BMG and is down-regulated after exposure of the cells to LPS. A phorbol ester induced a down-regulation of CD62L and blocked the LPS-induced expression of CD14. However, a metalloproteinase inhibitor (BB-3103) blocked the former but not the latter effect of PMA. We also observed an absence of cross-reactivity between LPS and a CD62L ligand (fucoidan) in binding studies with radiolabeled derivatives of the two agents. Furthermore, BMG froml-selectin-deficient mice expressed normal levels of CD14 in response to LPS. Taken together, these results demonstrate that in BMG, l-selectin is not the constitutive LPS receptor required for the LPS-induced expression of CD14.

RhoA/ROCK downregulates FPR2-mediated NADPH oxidase activation in mouse bone marrow granulocytes

2014 ◽  
Vol 26 (10) ◽  
pp. 2138-2146 ◽  
Author(s):  
Julia V. Filina ◽  
Aida G. Gabdoulkhakova ◽  
Valentina G. Safronova
Keyword(s):  
Bone Marrow ◽  
Nadph Oxidase ◽  
Mouse Bone Marrow ◽  
Nadph Oxidase Activation ◽  
Bone Marrow Granulocytes

Toll-like receptor 2-deficiency on bone marrow-derived cells augments vascular healing of murine arterial lesions

Life Sciences ◽  
2020 ◽  
Vol 242 ◽  
pp. 117189 ◽  
Author(s):  
W. Liu ◽  
J.-C. Eczko ◽  
M. Otto ◽  
R. Bajorat ◽  
B. Vollmar ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Toll Like Receptor ◽  
Arterial Lesions ◽  
Bone Marrow Derived Cells ◽  
Toll Like Receptor 2

scholarly journals Morphine Inhibits Murine Dendritic Cell IL-23 Production by Modulating Toll-like Receptor 2 and Nod2 Signaling

2011 ◽  
Vol 286 (12) ◽  
pp. 10225-10232 ◽  
Author(s):  
Jinghua Wang ◽  
Jing Ma ◽  
Rick Charboneau ◽  
Roderick Barke ◽  
Sabita Roy
Keyword(s):  
Dendritic Cells ◽  
Critical Role ◽  
Lipoteichoic Acid ◽  
Primary Response ◽  
Mouse Bone Marrow ◽  
Toll Like Receptor ◽  
Tlr2 Ligand ◽  
Tlr4 Ligand ◽  
Toll Like Receptor 2 ◽  
Activating Transcription Factor

IL-23, produced by dendritic cells (DCs) and macrophages, plays a critical role in innate immunity against bacterial infection. Our previous studies show that morphine disrupts the IL-23/IL-17 mediated pulmonary mucosal host defense and increases susceptibility to Streptococcus pneumoniae lung infection. To determine the mechanism by which morphine modulates IL-23 production, mouse bone marrow-derived dendritic cells (BMDCs) and macrophages (BMDMs) were treated with morphine, and infected with S. pneumoniae or stimulated with Toll-like receptor (TLR) and Nod2 ligands. We found that a significant increase in IL-23 protein production was observed in S. pneumoniae, TLR2 ligand lipoteichoic acid (LTA), and TLR4 ligand pneumolysin (PLY) stimulated BMDCs and BMDMs. Interestingly, although Nod2 ligand muramyldipeptide (MDP) alone had no effect on IL-23 production, it potentiated LTA induced IL-23 production to the same level as that observed following S. pneumoniae infection, suggesting that S. pneumoniae induced IL-23 production in DCs involves activation of both TLR2 and Nod2 signaling mechanisms. Furthermore, pretreatment of DCs with MyD88 (myeloid differentiation primary response gene 88) and IL-1 receptor-associated kinase (IRAK) 1/4 inhibitors, or TLR2 antibody diminished the S. pneumoniae induced IL-23 and abolished the inhibitory effects of morphine, indicating that S. pneumoniae induced IL-23 production depends on activation of the TLR2-MyD88-IRAK1/4 signaling pathway. Moreover, morphine decreased S. pneumoniae induced phosphorylation of interferon regulatory factor 3 (IRF3) and activating transcription factor 2 in DCs. Taken together, our study shows that morphine impairs S. pneumoniae induced IL-23 production through MyD88-IRAK1/4-dependent TLR2 and Nod2 signaling in DCs.

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