scholarly journals Regulation of Chemokines, CCL3 and CCL4, by Interferon γ and Nitric Oxide Synthase 2 in Mouse Macrophages and During Salmonella enterica Serovar Typhimurium Infection

2013 ◽  
Vol 207 (10) ◽  
pp. 1556-1568 ◽  
Author(s):  
Bhagawat Chandrasekar ◽  
Mukta Deobagkar-Lele ◽  
Emmanuel S. Victor ◽  
Dipankar Nandi
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Salmonella Enterica ◽  
Salmonella Enterica Serovar Typhimurium ◽  
Interferon Γ ◽  
Mouse Macrophages ◽  
Serovar Typhimurium ◽  
Nitric Oxide Synthase 2 ◽  
Oxide Synthase

scholarly journals Nitric oxide regulates nitric oxide synthase-2 gene expression by inhibiting NF-κB binding to DNA

1997 ◽  
Vol 322 (2) ◽  
pp. 609-613 ◽  
Author(s):  
Song Kyu PARK ◽  
Hsin Lee LIN ◽  
Sean MURPHY
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Interferon Γ ◽  
No Production ◽  
No Donor ◽  
Nitric Oxide Synthase 2 ◽  
Oxide Synthase ◽  
Spermine Nonoate ◽  
Dna Complex

Treatment of astroglial cells with interleukin 1β and interferon γ transcriptionally activates the nitric oxide synthase (NOS)-2 gene. The duration of mRNA expression is brief because of transcript instability. In addition, NO donors reduce the expression of NOS-2 mRNA dramatically by reducing the rate of transcription. In this study we observed that the NO donor, spermine NONOate did not inhibit the activation and translocation of NF-κB, a key transcription factor in the induction of NOS-2, but inhibited formation of the NF-κB–DNA complex. This effect was reversed by methaemoglobin (acting as an NO trap) and by the reducing agent dithiothreitol. Formation of the interferon-regulatory factor–DNA complex was unaffected by NO. These results suggest that NO can modulate its own production by interfering with NF-κB interaction with the promoter region of the NOS gene, a negative feedback effect that may be important for limiting NO production in vivo.

Retinoic Acid Inhibits Nitric Oxide Synthase-2 Expression through the Retinoic Acid Receptor-α

2000 ◽  
Vol 270 (3) ◽  
pp. 846-851 ◽  
Author(s):  
Allan Sirsjö ◽  
Andreas C Gidlöf ◽  
Anneli Olsson ◽  
Hans Törmä ◽  
Mikko Ares ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Retinoic Acid ◽  
Nitric Oxide Synthase ◽  
Retinoic Acid Receptor ◽  
Acid Receptor ◽  
Retinoic Acid Receptor Α ◽  
Nitric Oxide Synthase 2 ◽  
Oxide Synthase

Deficiency of Nitric Oxide Synthase 2 Results in Increased Neointima Formation in a Mouse Model of Vascular Injury

2003 ◽  
Vol 41 (6) ◽  
pp. 897-902 ◽  
Author(s):  
Allan Sirsjö ◽  
Anders Löfving ◽  
Göran K. Hansson ◽  
Dick Wågsäter ◽  
Shinichi Tokuno ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Mouse Model ◽  
Vascular Injury ◽  
Neointima Formation ◽  
Nitric Oxide Synthase 2 ◽  
Oxide Synthase

scholarly journals Nitric-oxide Synthase-2 Linkage to Focal Adhesion Kinase in Neutrophils Influences Enzyme Activity and β2Integrin Function

2013 ◽  
Vol 288 (7) ◽  
pp. 4810-4818 ◽  
Author(s):  
Stephen R. Thom ◽  
Veena M. Bhopale ◽  
Tatyana N. Milovanova ◽  
Ming Yang ◽  
Marina Bogush ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Enzyme Activity ◽  
Nitric Oxide Synthase ◽  
Focal Adhesion Kinase ◽  
Focal Adhesion ◽  
Nitric Oxide Synthase 2 ◽  
Oxide Synthase

scholarly journals The nitric oxide synthase 2 pathway is targeted by both pro- and anti-inflammatory treatments in the immature human intestine

Nitric Oxide ◽  
2017 ◽  
Vol 66 ◽  
pp. 53-61 ◽  
Author(s):  
Emanuela Ferretti ◽  
Eric Tremblay ◽  
Marie-Pier Thibault ◽  
David Grynspan ◽  
Karolina M. Burghardt ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Human Intestine ◽  
Anti Inflammatory ◽  
Nitric Oxide Synthase 2 ◽  
Oxide Synthase

scholarly journals Expression of the Nitric Oxide Synthase 2 Gene Is Not Essential for Early Control of Mycobacterium tuberculosis in the Murine Lung

2000 ◽  
Vol 68 (12) ◽  
pp. 6879-6882 ◽  
Author(s):  
Andrea M. Cooper ◽  
John E. Pearl ◽  
Jason V. Brooks ◽  
Stefan Ehlers ◽  
Ian M. Orme
Keyword(s):  
Nitric Oxide ◽  
Mycobacterium Tuberculosis ◽  
Nitric Oxide Synthase ◽  
Low Dose ◽  
Interleukin 12 ◽  
Infection Model ◽  
Rapid Progression ◽  
Ifn Γ ◽  
Nitric Oxide Synthase 2 ◽  
Oxide Synthase

ABSTRACT The interleukin-12 and gamma interferon (IFN-γ) pathway of macrophage activation plays a pivotal role in controlling tuberculosis. In the murine model, the generation of supplementary nitric oxide by the induction of the nitric oxide synthase 2 (NOS2) gene product is considered the principal antimicrobial mechanism of IFN-γ-activated macrophages. Using a low-dose aerosol-mediated infection model in the mouse, we have investigated the role of nitric oxide in controllingMycobacterium tuberculosis in the lung. In contrast to the consequences of a systemic infection, a low dose of bacteria introduced directly into the lungs of mice lacking the NOS2 gene is controlled almost as well as in intact animals. This is in contrast to the rapid progression of disease in mice lacking IFN-γ or a key member of the IFN signaling pathway, interferon regulatory factor 1. Thus while IFN-γ is pivotal in early control of bacterial growth in the lung, this control does not completely depend upon the expression of the NOS2 gene. The absence of inducible nitric oxide in the lung does, however, result in increased polymorphonuclear cell involvement and eventual necrosis in the pulmonary granulomas of the infected mice lacking the NOS2 gene.

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