Folia Parasitologica 60 213-217 (2013) | DOI: 10.14411/fp.2013.023
Abstract: The host immune response to parasitic infections plays an important role in controlling multiplication of the parasite and reducing clinical symptoms and life-threatening complications. Nitric oxide (NO), an important innate immune factor and classic Th1 immune effector, may play a role in inhibiting plasmodium infection. In this study, we used two different approaches (L-Arginine [precursor of NO] and NOC5 [short-time NO donor]) to prove the roles of NO in malaria infection. We used 6-8 week-old female BALB/c mice infected with the rodent malaria Plasmodium yoelii Landau, Michel et Adam, 1968 - strain 17XL (P.y17XL) - as a model. For L-Arg treatment, mice were administered with an oral dose of 1.5 mg/g L-Arg daily for seven consecutive days prior to infection with P.y17XL. L-Arg pretreatment resulted in the decrease of the mRNA level of the apical membrane antigen 1 (AMA1) gene, which encodes a protein involved in host invasion. For NOC5 treatment, NOC5 was injected intraperitoneally into the P.y17XL infected mice on day 5 post-infection or incubated in vitro with purified P.y17XL schizonts. Both in vivo and in vitro treatments with NOC5 led to down-regulation of the transcript and protein levels of invasion-related molecules (AMA1, merozoites surface protein 1 and Py235). Our results confirmed the protective role of NO in the asexual blood stage of parasitic infection, which may be partially due to reduced expression of parasite invasion molecules.
Received: September 28, 2012; Accepted: February 4, 2013; Published: July 23, 2013