Trypanosoma cruzi Infection Induces Myocardial Nitric Oxide Synthase

1997 ◽  
Vol 6 (3) ◽  
pp. 161-166 ◽  
Author(s):  
Huan Huang, MD ◽  
John Chan, MD ◽  
Murray Wittner, MD, PhD ◽  
Louis M Weiss, MD, MPH ◽  
J Bacchi, PhD ◽  
...  

2018 ◽  
Vol 129 ◽  
pp. 227-236 ◽  
Author(s):  
Amanda A. Felizardo ◽  
Ivo S. Caldas ◽  
Andréa A.S. Mendonça ◽  
Reggiani V. Gonçalves ◽  
Fernanda L. Tana ◽  
...  


2005 ◽  
Vol 66 (8) ◽  
pp. 68
Author(s):  
Mercedes T. Fernandez-Mestre ◽  
Eva Salazar ◽  
Zulay E. Layrisse


Placenta ◽  
2017 ◽  
Vol 51 ◽  
pp. 116-117
Author(s):  
M.F. Triquell ◽  
E. Benizio ◽  
M.J. Moreira-Espinoza ◽  
J.C. Ramírez ◽  
L. Mezzano ◽  
...  




2004 ◽  
Vol 72 (7) ◽  
pp. 4081-4089 ◽  
Author(s):  
Kara L. Cummings ◽  
Rick L. Tarleton

ABSTRACT Immune control of many intracellular pathogens, including Trypanosoma cruzi, is reported to be dependent on the production of nitric oxide. In this study, we show that mice deficient in inducible nitric oxide synthase (iNOS or NOS2) exhibit resistance to T. cruzi infection that is comparable to that of wild-type mice. This is the case for two iNOS-deficient mouse strains, Nos2tm1Lau and Nos2 N5, infected with the Brazil or Tulahuen strain of T. cruzi. In all cases, blood parasitemia, tissue parasite load, and survival rates are similar between wild-type and iNOS-deficient mice. In contrast, both wild-type and Nos2tm1Lau mice died within 32 days postinfection when treated with the nitric oxide synthase inhibitor aminoguanidine. Increased transcription of NOS1 or NOS3 is not found in iNOS-knockout (KO) mice, indicating that the absence of nitric oxide production through iNOS is not compensated for by increased production of other NOS isoforms. However, Nos2tm1Lau mice exhibit enhanced expression of tumor necrosis factor alpha, interleukin-1, and macrophage inflammatory protein 1α compared to that of wild-type mice, and these alterations may in part compensate for the lack of iNOS. These results clearly show that iNOS is not required for control of T. cruzi infection in mice.



2019 ◽  
Vol 2019 ◽  
pp. 1-14
Author(s):  
Carolina Panis ◽  
Vanessa Jacob Victorino ◽  
Vera Lúcia Hideko Tatakihara ◽  
Rubens Cecchini ◽  
Luiz Vicente Rizzo ◽  
...  

Infection with the protozoan Trypanosoma cruzi causes Chagas disease and consequently leads to severe inflammatory heart condition; however, the mechanisms driving this inflammatory response have not been completely elucidated. Nitric oxide (NO) is a key mediator of parasite killing in T. cruzi-infected mice, and previous studies have suggested that leukotrienes (LTs) essentially regulate the NO activity in the heart. We used infected 5-lipoxygenase-deficient mice (5-LO−/−) to explore the participation of nitric oxide synthase isoforms, inducible (iNOS) and constitutive (cNOS), in heart injury, cytokine profile, and oxidative stress during the early stage of T. cruzi infection. Our evidence suggests that the cNOS of the host is involved in the resistance of 5-LO−/− mice during T. cruzi infection. iNOS inhibition generated a remarkable increase in T. cruzi infection in the blood and heart of mice, whereas cNOS inhibition reduced cardiac parasitism (amastigote nests). Furthermore, this inhibition associates with a higher IFN-γ production and lower lipid peroxidation status. These data provide a better understanding about the influence of NO-interfering therapies for the inflammatory response toward T. cruzi infection.





2008 ◽  
Vol 10 (14-15) ◽  
pp. 1558-1566 ◽  
Author(s):  
Fabiana S. Machado ◽  
Janeusa T. Souto ◽  
Marcos A. Rossi ◽  
Lisia Esper ◽  
Herbert B. Tanowitz ◽  
...  


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