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Infection and Immunity, September 2003, p. 4917-4924, Vol. 71, No. 9
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.9.4917-4924.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Mice Lacking Inducible Nitric Oxide Synthase Demonstrate Impaired Killing of Porphyromonas gingivalis

Robert Gyurko,1* Gabriel Boustany,1 Paul L. Huang,2 Alpdogan Kantarci,1 Thomas E. Van Dyke,1 Caroline A. Genco,1,3,4 and Frank C. Gibson III3

Department of Periodontology and Oral Biology, Goldman School of Dental Medicine, Boston University,1 Cardiovascular Research Center, Massachusetts General Hospital and Harvard Medical School,2 Section of Infectious Disease, Department of Medicine,3 Department of Microbiology, Boston University Medical Center, Boston, Massachusetts 021184

Received 10 March 2003/ Returned for modification 8 May 2003/ Accepted 17 June 2003

Porphyromonas gingivalis is a primary etiological agent of generalized severe periodontitis, and emerging data suggest the importance of reactive oxygen and nitrogen species in periodontal tissue damage, as well as in microbial killing. Since nitric oxide (NO) released from inducible NO synthase (iNOS) has been shown to possess immunomodulatory, cytotoxic, and antibacterial effects in experimental models, we challenged iNOS-deficient (iNOS-/-) mice with P. gingivalis by using a subcutaneous chamber model to study the specific contribution of NO to host defense during P. gingivalis infection. iNOS-/- mice inoculated with P. gingivalis developed skin lesions and chamber rejection with higher frequency and to a greater degree than similarly challenged C57BL/6 wild-type (WT) mice. Chamber fluid from iNOS-/- mice possessed significantly more P. gingivalis than that of WT mice. The immunoglobulin G responses to P. gingivalis in serum was similar in WT and iNOS-/- mice, and the inductions of tumor necrosis factor alpha, interleukin-1ß and interleukin-6, and prostaglandin E2 were comparable between the two mouse strains. Although no differences in total leukocyte counts in chamber fluids were observed between iNOS-/- and WT mice, the percentage of dead polymorphonuclear leukocytes (PMNs) was significantly greater in iNOS-/- mouse chamber fluids than that of WT samples. Interestingly, casein-elicited PMNs from iNOS-/- mice released more superoxide than did WT PMNs when stimulated with P. gingivalis. These results indicate that modulation of superoxide levels is a mechanism by which NO influences PMN function and that NO is an important element of the host defense against P. gingivalis.

* Corresponding author. Mailing address: Department of Periodontology and Oral Biology, Goldman School of Dental Medicine, Boston University, 100 East Newton St., Boston, MA 02118. Phone: (617) 638-4774. Fax: (617) 638-4799. E-mail: gyurko{at}bu.edu.

Editor: J. N. Weiser

Infection and Immunity, September 2003, p. 4917-4924, Vol. 71, No. 9
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.9.4917-4924.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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