Reactive Nitrogen Species Contribute to Innate Host Defense againstCampylobacter jejuni

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 marrowderived 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.

A BODIPY fluorescence probe modulated by selenoxide spirocyclization reaction for peroxynitrite detection and imaging in living cells

“…We chose the mouse macrophage cell line RAW264.7 as a model cell line, because the macrophage cells activate the generation of reactive oxygen and nitrogen species after exposure to lipopolysaccharide (LPS)/interferon-g (IFN-g) and phorbol 12-myristate 13-acetate (PMA) [41]. RAW264.…”

Study of exogenous oxidative stress response in Escherichia coli, Pseudomonas spp., Bacillus spp., and Salmonella spp.

“…Autoxidation of reduced FAD or reduced flavoprotein gives rise to •OH, and the enzyme NADPH oxidase can also generate O 2 -and H 2 O 2 (Cabiscol et al, 2000;Moat et al, 2002). The reaction of O 2 -with nitric oxide forms peroxynitrite anion, which is highly reactive with certain amino acid residues of proteins, which in turn induces the formation of other toxic derivatives within bacterial cells (Squadritoa et al, 1998;Cabiscol et al, 2000;Schutter and Dick, 2000;Moat et al, 2002;Kamat, 2006;Iovine et al, 2008).…”

Molecular mechanisms and biological role ofCampylobacter jejuniattachment to host cells

“…Inactivation of N-linked glycosylation machinery leads to decreased colonisation ability of bacteria, as well as to a reduction of adherence to and invasion of human epithelial cells suggesting that some of these glycoproteins may play a role of adhesins [57][58][59][60]. Although it remains unknown whether Campylobacter N-glycosylation is required for adhesion there is some evidence that it might influence host immune response [61,62].…”

“…In addition to galactose-specific C-type lectins described above, other C-type lectins as well as sialic acidbinding immunoglobulin-like lectins (siglecs) may be involved in host-pathogen interaction [61,62]. Siglecs are a family of type I membrane proteins widely expressed on immune cells that have specificity for sialic acid-containing glycans present in some types of Campylobacter lipo-oligosaccharides (LOSs).…”