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Differences in cNOS/iNOS Activity during Resistance to Trypanosoma cruzi Infection in 5-Lipoxygenase Knockout Mice. | LitMetric

AI Article Synopsis

  • - Chagas disease, caused by a protozoan infection, leads to severe heart inflammation, but the exact mechanisms of this inflammatory response are still unclear.
  • - The study investigates the roles of two nitric oxide synthase isoforms, inducible (iNOS) and constitutive (cNOS), in heart injury and immune response using a specific type of mouse that lacks 5-lipoxygenase (5-LO).
  • - Results show that while inhibiting iNOS increased infection levels in the mice, inhibiting cNOS reduced heart parasitism and improved immune responses, indicating the importance of NO modulation in managing heart inflammation during Chagas disease.

Article Abstract

Infection with the protozoan 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 -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 infection. Our evidence suggests that the cNOS of the host is involved in the resistance of 5-LO mice during infection. iNOS inhibition generated a remarkable increase in infection in the blood and heart of mice, whereas cNOS inhibition reduced cardiac parasitism (amastigote nests). Furthermore, this inhibition associates with a higher IFN- production and lower lipid peroxidation status. These data provide a better understanding about the influence of NO-interfering therapies for the inflammatory response toward infection.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6854994PMC
http://dx.doi.org/10.1155/2019/5091630DOI Listing

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