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Infection and Immunity, March 2008, p. 986-993, Vol. 76, No. 3
0019-9567/08/$08.00+0     doi:10.1128/IAI.01063-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Reactive Nitrogen Species Contribute to Innate Host Defense against Campylobacter jejuni{triangledown}

Nicole M. Iovine,1,2* Seema Pursnani,2 Alex Voldman,1 Gregory Wasserman,3 Martin J. Blaser,1,2 and Yvette Weinrauch1

Department of Microbiology, New York University School of Medicine, 550 First Avenue, New York, New York 10016,1 Department of Medicine, New York University School of Medicine, 550 First Avenue, New York, New York 10016,2 University of Vermont, 85 South Prospect Street, Burlington, Vermont 054053

Received 1 August 2007/ Returned for modification 4 October 2007/ Accepted 20 December 2007

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.

* Corresponding author. Mailing address: New York University School of Medicine at the Veteran's Administration Medical Center, 423 East 23rd St., Room 6005AW, New York, NY 10010. Phone: (212) 263-4239. Fax: (212) 263-4108. E-mail: iovinn01{at}med.nyu.edu

{triangledown} Published ahead of print on 3 January 2008.

Editor: V. J. DiRita

Infection and Immunity, March 2008, p. 986-993, Vol. 76, No. 3
0019-9567/08/$08.00+0     doi:10.1128/IAI.01063-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

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