Original Paper

Parasitology Research

, Volume 100, Issue 6, pp 1341-1350

Nitric oxide contributes to host resistance against experimental Taenia crassiceps cysticercosis

  • Javier Alonso-TrujilloAffiliated withLaboratory of Immunoparasitology, Unidad de Biomedicina, Facultad de Estudios Superiores-Iztacala, Universidad Nacional Autónoma de México
  • , Irma Rivera-MontoyaAffiliated withLaboratory of Immunoparasitology, Unidad de Biomedicina, Facultad de Estudios Superiores-Iztacala, Universidad Nacional Autónoma de México
  • , Miriam Rodríguez-SosaAffiliated withLaboratory of Immunoparasitology, Unidad de Biomedicina, Facultad de Estudios Superiores-Iztacala, Universidad Nacional Autónoma de México
  • , Luis I. TerrazasAffiliated withLaboratory of Immunoparasitology, Unidad de Biomedicina, Facultad de Estudios Superiores-Iztacala, Universidad Nacional Autónoma de México Email author 

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Abstract

The immune mechanisms that underlie resistance and susceptibility to cysticercosis are not completely understood. In this paper, using susceptible BALB/c mice and resistant STAT6−/− BALB/c mice, we have analyzed the role of nitric oxide (NO) in determining the outcome of murine cysticercosis caused by the cestode Taenia crassiceps. After T. crassiceps infection, wild-type BALB/c mice developed a strong Th2-like response, produced high levels of IgG1, IgE, IL-5, IL-4, and discrete levels of NO, and remained susceptible to T. crassiceps infection. In contrast, similarly infected BALB/c mice treated with \( N^{{\text{ $ \omega $ }}} \)-nitro-l-arginine methyl ester (l-NAME, an inhibitor of NO synthase) mounted a similar immune response but with lower levels of NO and harbored nearly 100% more parasites than \( N^{{\text{ $ \omega $ }}} \)-nitro-d-arginine methyl ester (d-NAME, inactive enantiomer)-treated mice. To further analyze the role of NO in murine cysticercosis, we treated STAT6−/− male mice (known to be highly resistant to T. crassiceps) with l-NAME during 8 weeks of infection. As expected, STAT6−/− mice mounted a strong Th1-like response, produced high levels of IgG2a, IFN-γ, and IL-17, whereas their macrophages displayed increased transcripts of tumor necrosis factor (TNF)-α as well as inducible nitric oxide synthase (iNOS) and efficiently controlled T. crassiceps infection. However, STAT6−/− male mice receiving l-NAME mounted a similar immune response but with lower iNOS transcripts concomitantly with decreased levels of NO in sera and displayed significantly higher parasite burdens. These findings suggest that macrophage activation and NO production are effector mechanisms that importantly contribute in host resistance to T. crassiceps infection.