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Infection and Immunity, February 2002, p. 679-684, Vol. 70, No. 2
0019-9567/01/$04.00+0 DOI: 70.2.679-684.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.
Division of Bacteriology, National Institute for Biological Standards and Control, South Mimms, Potters Bar, Hertfordshire, EN6 3QG,1 Department of Immunology and Bacteriology, University of Glasgow, Glasgow G11 6NT, United Kingdom2
Received 22 August 2001/ Returned for modification 20 September 2001/ Accepted 6 November 2001
The mechanism whereby whole-cell pertussis vaccines (WCV) confer protection against Bordetella pertussis is still not fully understood. We have previously reported that macrophage activation produced by vaccination with WCV is associated with induction of NO synthesis by macrophages in response to in vitro stimulation with B. pertussis antigens. To determine whether NO production is an effector of protection or simply a marker of activation, the susceptibility of inducible nitric oxide synthase (type II, iNOS) knockout mice to infection with B. pertussis was examined. We showed that iNOS knockout mice were more susceptible to B. pertussis respiratory challenge than wild-type mice. iNOS-deficient mice also developed a less effective protective response than wild-type mice after the same immunization with WCV. This suggests that NO plays an important role in effecting protection against B. pertussis challenge.
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