scholarly journals Inducible nitric oxide synthase in innate immune cells is important for restricting cyst formation of Toxoplasma gondii in the brain but not required for the protective immune process to remove the cysts

2018 ◽  
Vol 20 (4) ◽  
pp. 261-266 ◽  
Author(s):  
Qila Sa ◽  
Ashish Tiwari ◽  
Eri Ochiai ◽  
Jeremi Mullins ◽  
Yasuhiro Suzuki
Keyword(s):  
Nitric Oxide ◽  
Toxoplasma Gondii ◽  
Inducible Nitric Oxide Synthase ◽  
Immune Cells ◽  
Cyst Formation ◽  
Innate Immune ◽  
Innate Immune Cells ◽  
Oxide Synthase ◽  
The Brain ◽  
Inducible Nitric Oxide

scholarly journals DNA-based fluorescent probes of NOS2 activity in live brains

2020 ◽  
Vol 117 (26) ◽  
pp. 14694-14702 ◽  
Author(s):  
Aneesh T. Veetil ◽  
Junyi Zou ◽  
Katharine W. Henderson ◽  
Maulik S. Jani ◽  
Shabana M. Shaik ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Fluorescent Probes ◽  
Immune Cells ◽  
Innate Immune ◽  
Innate Immune Cells ◽  
Molecular Patterns ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Innate immune cells destroy pathogens within a transient organelle called the phagosome. When pathogen-associated molecular patterns (PAMPs) displayed on the pathogen are recognized by Toll-like receptors (TLRs) on the host cell, it activates inducible nitric oxide synthase (NOS2) which instantly fills the phagosome with nitric oxide (NO) to clear the pathogen. Selected pathogens avoid activating NOS2 by concealing key PAMPs from their cognate TLRs. Thus, the ability to map NOS2 activity triggered by PAMPs can reveal critical mechanisms underlying pathogen susceptibility. Here, we describe DNA-based probes that ratiometrically report phagosomal and endosomal NO, and can be molecularly programmed to display precise stoichiometries of any desired PAMP. By mapping phagosomal NO produced in microglia of live zebrafish brains, we found that single-stranded RNA of bacterial origin acts as a PAMP and activates NOS2 by engaging TLR-7. This technology can be applied to study PAMP−TLR interactions in diverse organisms.

Toxoplasma gondii: in vivo expression of BAG-5 and cyst formation is independent of TNF p55 receptor and inducible nitric oxide synthase functions

2002 ◽  
Vol 4 (3) ◽  
pp. 261-270 ◽  
Author(s):  
Neide M. Silva ◽  
Wagner L. Tafuri ◽  
Jacqueline I. Alvarez-Leite ◽  
José R. Mineo ◽  
Ricardo T. Gazzinelli
Keyword(s):  
Nitric Oxide ◽  
Toxoplasma Gondii ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Cyst Formation ◽  
In Vivo Expression ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Isoflurane Preconditioning Induces Neuroprotection That Is Inducible Nitric Oxide Synthase–dependent in Neonatal Rats

2004 ◽  
Vol 101 (3) ◽  
pp. 695-703 ◽  
Author(s):  
Ping Zhao ◽  
Zhiyi Zuo
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Weight Ratio ◽  
Cerebral Hemispheres ◽  
Brain Hypoxia ◽  
Hypoxia Ischemia ◽  
Oxide Synthase ◽  
The Brain ◽  
Inducible Nitric Oxide

Background Perinatal stroke is a common human disease. Neonatal brains are immature and engaged in active synaptogenesis. Preconditioning adult rats with the volatile anesthetic isoflurane induces neuroprotection. Whether isoflurane preconditioning induces neuroprotection in neonates is not known. Methods Seven-day-old Sprague-Dawley rats had left common carotid arterial ligation followed by hypoxia with 8% oxygen for 1, 2, or 2.5 h at 37 degrees C. Isoflurane preconditioning with 1 or 1.5% isoflurane for 30 min was performed at 24 h before the brain hypoxia/ischemia. The inducible nitric oxide synthase inhibitor aminoguanidine (200 mg/kg, intraperitoneally) was administered 30 min before the isoflurane pretreatment. The weight ratio of left to right cerebral hemispheres at 7 days after the brain hypoxia/ischemia was calculated. The mortality during the period from cerebral hypoxia/ischemia to 7 days afterwards was monitored. In another experiment, 6-day-old rats were exposed to 1.5% isoflurane for 30 min. The cerebral hemispheres were removed at various time points for Western analysis of inducible nitric oxide synthase. Results The mortality was about 40% in neonates with brain hypoxia/ischemia for 2 h or 2.5 h and was not altered by isoflurane preconditioning. The weight ratio of left/right cerebral hemispheres in the survivors was 0.99 +/- 0.02, 0.65 +/- 0.19, and 0.86 +/- 0.15 (n = 7-18) for the rats in control, brain hypoxia/ischemia for 2.5 h, and isoflurane preconditioning plus brain hypoxia/ischemia for 2.5 h groups, respectively (P < 0.05 for the comparisons between control versus brain hypoxia/ischemia and brain hypoxia/ischemia versus isoflurane preconditioning plus brain hypoxia/ischemia). This isoflurane preconditioning-induced neuroprotection was abolished by aminoguanidine (the weight ratio was 0.61 +/- 0.18, n = 12). Isoflurane induced a time-dependent increase in the inducible nitric oxide synthase proteins. Conclusions Isoflurane preconditioning induces neuroprotection in neonatal rats. This neuroprotection is inducible nitric oxide synthase-dependent.

scholarly journals Isoflurane Preconditioning Improves Long-term Neurologic Outcome after Hypoxic–Ischemic Brain Injury in Neonatal Rats

2007 ◽  
Vol 107 (6) ◽  
pp. 963-970 ◽  
Author(s):  
Ping Zhao ◽  
Longyun Peng ◽  
Liaoliao Li ◽  
Xuebing Xu ◽  
Zhiyi Zuo
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Brain Ischemia ◽  
Neurologic Outcome ◽  
Hypoxia Ischemia ◽  
Oxide Synthase ◽  
The Brain ◽  
Inducible Nitric Oxide

Background Preconditioning the brain with relatively safe drugs seems to be a viable option to reduce ischemic brain injury. The authors and others have shown that the volatile anesthetic isoflurane can precondition the brain against ischemia. Here, the authors determine whether isoflurane preconditioning improves long-term neurologic outcome after brain ischemia. Methods Six-day-old rats were exposed to 1.5% isoflurane for 30 min at 24 h before the brain hypoxia-ischemia that was induced by left common carotid arterial ligation and then exposure to 8% oxygen for 2 h. The neuropathology, motor coordination, and learning and memory functions were assayed 1 month after the brain ischemia. Western analysis was performed to quantify the expression of the heat shock protein 70, Bcl-2, and survivin 24 h after isoflurane exposure. Results The mortality was 45% after brain hypoxia-ischemia. Isoflurane preconditioning did not affect this mortality. However, isoflurane preconditioning attenuated ischemia-induced loss of neurons and brain tissues, such as cerebral cortex and hippocampus in the survivors. Isoflurane also improved the motor coordination of rats at 1 month after ischemia. The learning and memory functions as measured by performance of Y-maze and social recognition tasks in the survivors were not affected by the brain hypoxia-ischemia or isoflurane preconditioning. The expression of Bcl-2, a well-known antiapoptotic protein, in the hippocampus is increased after isoflurane exposure. This increase was reduced by the inhibitors of inducible nitric oxide synthase. Inducible nitric oxide synthase inhibition also abolished isoflurane preconditioning-induced neuroprotection. Conclusions Isoflurane preconditioning improved the long-term neurologic outcome after brain ischemia. Inducible nitric oxide synthase may be involved in this neuroprotection.

Human Immunodeficiency Virus-1–Infected Macrophages Induce Inducible Nitric Oxide Synthase and Nitric Oxide (NO) Production in Astrocytes: Astrocytic NO as a Possible Mediator of Neural Damage in Acquired Immunodeficiency Syndrome

Blood ◽  
1999 ◽  
Vol 93 (6) ◽  
pp. 1843-1850 ◽  
Author(s):  
Kotaro Hori ◽  
Parris R. Burd ◽  
Keizo Furuke ◽  
Joseph Kutza ◽  
Karis A. Weih ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Human Immunodeficiency Virus ◽  
Inducible Nitric Oxide Synthase ◽  
Inos Expression ◽  
No Production ◽  
Immunodeficiency Virus ◽  
Oxide Synthase ◽  
The Brain ◽  
Hiv 1 ◽  
Inducible Nitric Oxide

Nitric oxide (NO) plays an important role in normal neural cell function. Dysregulated or overexpression of NO contributes to neurologic damage associated with various pathologies, including human immunodeficiency virus (HIV)-associated neurological disease. Previous studies suggest that HIV-infected monocyte-derived macrophages (MDM) produce low levels of NO in vitro and that inducible nitric oxide synthase (iNOS) is expressed in the brain of patients with neurologic disease. However, the levels of NO could not account for the degree of neural toxicity observed. In this study, we found that induction of iNOS with concomitant production of NO occurred in primary human astrocytes, but not in MDM, when astrocytes were cocultured with HIV-1–infected MDM. This coincided with decreased HIV replication in infected MDM. Supernatants from cocultures of infected MDM and astrocytes also stimulated iNOS/NO expression in astrocytes, but cytokines known to induce iNOS expression (interferon-γ, interleukin-1β, and tumor necrosis factor-) were not detected. In addition, the recombinant HIV-1 envelope protein gp41, but not rgp120, induced iNOS in cocultures of uninfected MDM and astrocytes. This suggests that astrocytes may be an important source of NO production due to dysregulated iNOS expression and may constitute one arm of the host response resulting in suppression of HIV-1 replication in the brain. It also leads us to speculate that neurologic damage observed in HIV disease may ensue from prolonged, high level production of NO.

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