HIF-1α Regulation of Cytokine Production following TLR3 Engagement in Murine Bone Marrow–Derived Macrophages Is Dependent on Viral Nucleic Acid Length and Glucose Availability

2021 ◽  
pp. ji2001282
Author(s):  
Duale Ahmed ◽  
Allan Humphrey ◽  
David Roy ◽  
Mary-Elizabeth Sheridan ◽  
Zoya Versey ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Nucleic Acid ◽  
Cytokine Production ◽  
Viral Nucleic Acid ◽  
Murine Bone Marrow ◽  
Glucose Availability

scholarly journals The immunostimulatory activity of polysaccharides from Glycyrrhiza uralensis

PeerJ ◽  
2020 ◽  
Vol 8 ◽  
pp. e8294 ◽  
Author(s):  
Adila Aipire ◽  
Mahepali Mahabati ◽  
Shanshan Cai ◽  
Xianxian Wei ◽  
Pengfei Yuan ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Mouse Model ◽  
Side Effect ◽  
Cytokine Production ◽  
Human Monocyte ◽  
Glycyrrhiza Uralensis ◽  
Naive Mouse ◽  
Immunostimulatory Activity ◽  
Murine Bone Marrow ◽  
Tnf Α

Background The enhancement of immunity is very important for immunocompromised patients such as cancer patients with radiotherapy or chemotherapy. Glycyrrhiza uralensis has been used as food and medicine for a long history. G. uralensis polysaccharides (GUPS) were prepared and its immunostimulatory effects were investigated. Methods Human monocyte-derived dendritic cells (DCs) and murine bone marrow-derived DCs were treated with different concentrations of GUPS. The DCs maturation and cytokine production were analyzed by flow cytometry and ELISA, respectively. Inhibitors and Western blot were used to study the mechanism of GUPS. The immunostimulatory effects of GUPS were further evaluated by naïve mouse model and immunosuppressive mouse model induced by cyclophosphamide. Results GUPS significantly promoted the maturation and cytokine secretion of human monocyte-derived DCs and murine bone marrow-derived DCs through TLR4 and down-stream p38, JNK and NF-κB signaling pathways. Interestingly, the migration of GUPS treated-DCs to lymph node was increased. In the mouse model, GUPS increased IL-12 production in sera but not for TNF-α. Moreover, GUPS ameliorated the side effect of cyclophosphamide and improved the immunity of immunosuppressive mice induced by cyclophosphamide. These results suggested that GUPS might be used for cancer therapy to ameliorate the side effect of chemotherapy and enhance the immunity.

scholarly journals Sphingosine-1-Phosphate Receptor 2 Controls Podosome Components Induced by RANKL Affecting Osteoclastogenesis and Bone Resorption

Cells ◽  
2019 ◽  
Vol 8 (1) ◽  
pp. 17 ◽  
Author(s):  
Li-Chien Hsu ◽  
Sakamuri V. Reddy ◽  
Özlem Yilmaz ◽  
Hong Yu
Keyword(s):  
Bone Marrow ◽  
Bone Resorption ◽  
Bone Loss ◽  
Cytokine Production ◽  
Bone Marrow Cells ◽  
Proinflammatory Cytokine Production ◽  
Murine Bone Marrow ◽  
Sphingosine 1 Phosphate ◽  
Production Cell ◽  
Cell Chemotaxis

Proinflammatory cytokine production, cell chemotaxis, and osteoclastogenesis can lead to inflammatory bone loss. Previously, we showed that sphingosine-1-phosphate receptor 2 (S1PR2), a G protein coupled receptor, regulates inflammatory cytokine production and osteoclastogenesis. However, the signaling pathways regulated by S1PR2 in modulating inflammatory bone loss have not been elucidated. Herein, we demonstrated that inhibition of S1PR2 by a specific S1PR2 antagonist (JTE013) suppressed phosphoinositide 3-kinase (PI3K), mitogen-activated protein kinases (MAPKs), and nuclear factor kappa-B (NF-κB) induced by an oral bacterial pathogen, Aggregatibacter actinomycetemcomitans, and inhibited the release of IL-1β, IL-6, TNF-α, and S1P in murine bone marrow cells. In addition, shRNA knockdown of S1PR2 or treatment by JTE013 suppressed cell chemotaxis induced by bacteria-stimulated cell culture media. Furthermore, JTE013 suppressed osteoclastogenesis and bone resorption induced by RANKL in murine bone marrow cultures. ShRNA knockdown of S1PR2 or inhibition of S1PR2 by JTE013 suppressed podosome components, including PI3K, Src, Pyk2, integrin β3, filamentous actin (F-actin), and paxillin levels induced by RANKL in murine bone marrow cells. We conclude that S1PR2 plays an essential role in modulating proinflammatory cytokine production, cell chemotaxis, osteoclastogenesis, and bone resorption. Inhibition of S1PR2 signaling could be a novel therapeutic strategy for bone loss associated with skeletal diseases.

Deferoxamine B but Not Deferoxamine G1 Inhibits Cytokine Production in Murine Bone Marrow Macrophages

1995 ◽  
Vol 172 (2) ◽  
pp. 490-496 ◽  
Author(s):  
I. B. Autenrieth ◽  
E. Bohn ◽  
J. H. Ewald ◽  
J. Heesemann
Keyword(s):  
Bone Marrow ◽  
Cytokine Production ◽  
Murine Bone Marrow

Author response for "CXCR4, but not CXCR3, drives CD8 T-cell entry into and migration through the murine bone marrow"

2018 ◽  
Author(s):  
Marieke Goedhart ◽  
Stephanie Gessel ◽  
Robbert van der Voort ◽  
Edith Slot ◽  
Beth Lucas ◽  
...  
Keyword(s):  
Bone Marrow ◽  
T Cell ◽  
Cd8 T Cell ◽  
Cell Entry ◽  
Author Response ◽  
Murine Bone Marrow ◽  
And Migration

The diagnosis of hepatitis C viral infection

2014 ◽  
Vol 155 (26) ◽  
pp. 1019-1023
Author(s):  
Judit Gervain
Keyword(s):  
Hepatitis C ◽  
Nucleic Acid ◽  
Viral Infection ◽  
Structural Changes ◽  
Viral Infections ◽  
Transient Elastography ◽  
Viral Nucleic Acid ◽  
Length Of Treatment ◽  
Subtype B

The successful therapy of hepatitis C viral infection requires that the illness is diagnosed before the development of structural changes of the liver. Testing is stepwise consisting of screening, diagnosis, and anti-viral therapy follow-up. For these steps there are different biochemical, serological, histological and molecular biological methods available. For screening, alanine aminotransferase and anti-HCV tests are used. The diagnosis of infection is confirmed using real-time polymerase chain reaction of the viral nucleic acid. Before initiation of the therapy liver biopsy is recommended to determine the level of structural changes in the liver. Alternatively, transient elastography or blood biomarkers may be also used for this purpose. Differential diagnosis should exclude the co-existence of other viral infections and chronic hepatitis due to other origin, with special attention to the presence of autoantibodies. The outcome of the antiviral therapy and the length of treatment are mainly determined by the viral genotype. In Hungary, most patients are infected with genotype 1, subtype b. The polymorphism type that occurs in the single nucleotide located next to the interleukin 28B region in chromosome 19 and the viral polymorphism type Q80K for infection with HCV 1a serve as predictive therapeutic markers. The follow-up of therapy is based on the quantitative determination of viral nucleic acid according to national and international protocols and should use the same method and laboratory throughout the treatment of an individual patient. Orv. Hetil., 2014, 155(26), 1019–1023.

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