In vivo Inhibition of Nitric Oxide production leads to clinical and immunological improvement of hookworm infection
Document Type
Oral Presentation
Campus where you would like to present
SURC 137B
Start Date
17-5-2012
End Date
17-5-2012
Abstract
Hookworm infection is a major cause of anemia, malnutrition, growth delay and cognitive defects in resource poor countries. Human and animal studies suggest that infection with these intestinal nematodes is associated with impaired cellular immunity, characterized by reduced lymphocyte proliferation in response to both parasite and heterologous antigens. In vitro studies have shown that nitric oxide (NO) is one of the leading agent causing impaired cellular responses. Spleenocytes from infected hamsters secreted more NO in culture than did those from naive animals. In order to further identify the role of NO in hookworm pathogenesis and pathology, we conducted an experiment where the production of NO was inhibited using N-Monomethyl-L-Arginine (L-NAME). Hamsters were infected with 100 third stage larvae of the hookworm, Ancylostoma ceylanicum. Hamsters that received L-NAME showed lower worm burden (4 + 2) at day 36 post-infection (PI). The worm burden in the control group, without L-NAME was (21 + 4, p < 0.005). Similarly, the L-NAME group had lower egg count as from day 22 PI to day 36 PI. Anemia was assessed by measuring the hemoglobin levels and showed that the hamsters in the control group were more anemic. Together, these data suggest that NO modulates the clinical outcome of hookworm infection.
Recommended Citation
Berndt, Amanda, "In vivo Inhibition of Nitric Oxide production leads to clinical and immunological improvement of hookworm infection" (2012). Symposium Of University Research and Creative Expression (SOURCE). 71.
https://digitalcommons.cwu.edu/source/2012/oralpresentations/71
Additional Mentoring Department
Biological Sciences
In vivo Inhibition of Nitric Oxide production leads to clinical and immunological improvement of hookworm infection
SURC 137B
Hookworm infection is a major cause of anemia, malnutrition, growth delay and cognitive defects in resource poor countries. Human and animal studies suggest that infection with these intestinal nematodes is associated with impaired cellular immunity, characterized by reduced lymphocyte proliferation in response to both parasite and heterologous antigens. In vitro studies have shown that nitric oxide (NO) is one of the leading agent causing impaired cellular responses. Spleenocytes from infected hamsters secreted more NO in culture than did those from naive animals. In order to further identify the role of NO in hookworm pathogenesis and pathology, we conducted an experiment where the production of NO was inhibited using N-Monomethyl-L-Arginine (L-NAME). Hamsters were infected with 100 third stage larvae of the hookworm, Ancylostoma ceylanicum. Hamsters that received L-NAME showed lower worm burden (4 + 2) at day 36 post-infection (PI). The worm burden in the control group, without L-NAME was (21 + 4, p < 0.005). Similarly, the L-NAME group had lower egg count as from day 22 PI to day 36 PI. Anemia was assessed by measuring the hemoglobin levels and showed that the hamsters in the control group were more anemic. Together, these data suggest that NO modulates the clinical outcome of hookworm infection.
Faculty Mentor(s)
Blaise Dondji