Title

In vivo Inhibition of Nitric Oxide production leads to clinical and immunological improvement of hookworm infection

Presenter Information

Amanda Berndt

Document Type

Oral Presentation

Location

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.

Faculty Mentor(s)

Blaise Dondji

Additional Mentoring Department

Biological Sciences

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May 17th, 12:20 PM May 17th, 12:40 PM

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.