Abstract
Campylobacter jejuni
, a gram-negative, invasive organism, is a common cause of food-borne bacterial diarrheal disease. However, the relationship between
C. jejuni
and the innate immune system is not well described. To better characterize host defense against
C. jejuni
, we investigated the ability of nitric oxide/reactive nitrogen species to kill two strains of
C. jejuni. C. jejuni
viability was measured after exposure to reactive nitrogen species produced biochemically as acidified nitrite and by bone marrow-derived macrophages. We report that acidified nitrite caused a 3-log-increased kill of
C. jejuni
(
P
< 0.05) at doses that did not affect the viability of
Salmonella enterica
serovar Typhimurium. Expression of
NOS2
, the gene responsible for the production of inducible nitric oxide, was increased >100-fold in murine macrophages after incubation with
C. jejuni
(
P
< 0.001). These macrophages effected a 2-log-increased kill of
C. jejuni
over 24 h compared to that by NOS2
−/−
macrophages unable to produce nitric oxide (
P
< 0.05). These findings suggest that the mammalian host upregulates the production of nitric oxide in response to exposure to
C. jejuni
and that nitric oxide and reactive nitrogen species comprise part of the innate defense mechanisms that contribute to the resolution of
C. jejuni
infection.